The inheritance of resistance to Xanthomonas campestris pv. translucens (J.J.R.) Dowson in barley
by Gurbuz Mizrak
A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in Plant
Pathology
Montana State University
© Copyright by Gurbuz Mizrak (1985)
Abstract:
Inheritance of resistance to bacterial leaf streak was investigated in 23 barley cultivars. Parents, F1s
and F2s of one complete dialiel set with six varieties and those of 23 other crosses were tested with one
Montana isolate (X-67) of Xanthomonas campestris pv. translucens in the field. An inoculation method
is described which result in a uniform level of infection.
Barley cultivars, Herta, Summit, Oderbrucker, Betzes, Alpine, Luther, CI 12558, CI 12569, CI 12595,
CI 12777, CI 12787, CI 12866, CI 13095, PI 382511, PI 382650, PI 382720, PI 382732, and PI 383077
were found to be promising sources for resistance to bacterial leaf streak. Resistance in these cultivars
varied with regard to gene action and number. Some of them may have identical genes or differrent
genes in the same chromosomes. Further study is needed to determine identical, linked, and
independent genes. Also, a close relation, wich suggests a linkage, was found between earliness and
susceptibility. THE INHERITANCE OF RESISTANCE TO Xanthomonas campestris
pv. translucens (J.J.R.) DOWSON IN BARLEY
by
Gur buz
Mizrak
A th e s is su b m itted . in p a r t i a l f u lf illm e n t
of the r e q u i r e m e n t s f o r the degree
of
' Master
of
Science
in
Plant
Pathology
MONTANA STATE UNIVERSITY
^ o z e m a n , Mo n t a n a
Ma r c h I 9 85
APPROVAL
of
a thesis
submitted
by
G i i r buz Miz r a k
T h i s t h e s i s h a s b e e n r e a d by e a c h m e m b e r o f t h e
t h e s i s c o m m i t t e e a n d h a s b e e n f o u n d t o be s a t i s f a c t o r y
regarding content,
English usage, form at,
citations,
b i b l i o g r a p h i c s t y l e , and c o n s i s t e n c y , and i s r e a d y f o r
s u b m i s s i o n to the College of G ra d ua t e S t u d i e s .
Date
Approved
Dat e
for
Ma j o r
Department
He ad , Ma j o r
Approved f o r
the
College
Depa r t me'n t
of Graduat e
j ' Z a ^ S' j —
Da t e
Graduate
Dean
Studies
iii
STATEMENT OF PERMISSION TO USE
In
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requirments
this
for
I
available
borrowers
quotations
permission,
source
is
agree
from
professor,
Libraries
under
thesis
provided
of
or
when,
the
copying
the
partial
degree
at
Library
rules
of
fulfillment
Montana S t a t e
shall
the
make
Library.
are allowable without
that
accurate
of
it
Brief
special
acknowledgment
of
made.
reproduction
of
that
this
Perm ission
use
in
a m aster's
University,
to
thesis
or
financial
for
extensive
this
thesis
in
his
in
the
m aterials
use
gain
permission.
Signature
Date___ /l/frAArJ) .C
of
shall
ma y
absence,
opinion
is
the
not
for
quotation
be
granted
by
the
scholarly
be a l l o w e d
in
by
the
without
of
proposed
purposes.
this
or
major
D irector
of e i t h e r ,
m aterial
from
thesis
Any
for
my w r i t t e n
In d e d i c a t i o n
to:
My d a u g h t e r s Tu g b a a n d G a y e ,
my w i f e , my f a t h e r and m o t h e r
V
VITA
GUrbUz
on F e b r u a r y
up i n
Mizrak,
2,
son of Huseyi n
1949 i n
Inziloglu
and
graduated
November
June
I 972 w i t h
Gur buz
in
from
1967,
A griculture,
Ankara,
he
wa s
born
Turkey.
He g r e w
h i s se c o n d e r y e d u c a t i o n i n
Ankara,
his
father
Gazi
High
farmed.
School
started
attending
the U n iv e rsity
of Ankara,
a Bachelor
worked
the
I n z i l o g l u f Ankara,
where
Gurbuz r e c e i v e d
a n d Me mduha ,
for
of
the
Agricultural
Science
Seed
in
June
the
1967.
In
Faculty
of
and g r a d u a t e d i n
degree
in
Certification
Research
Institutes
Agr o n o my .
Institute
in
Ankar a
a n d A d a p a z a r i . He w o r k e d a s a t r a i n e e i n W e s t G e r m a n y a n d
CIMMYT
in
Mexico.
Graduate
School
complete
a Master
of
In
March
1983,
Gurbuz
Montana
State
Universiy
of S c i e n c e
degree
in
Mar ch
entered
and
1985.
the
will
vi
ACKNOWLEDGEMENT
I
wish
major
of
this
acknowledge
professor,
professional
years
to
Dr.
guidance
study
and
David
and
C.
Sands
willing
my t h a n k s
for
his
assistance
research,and
in
the
help,
during
the
preparation
of
Sharp,
D.
thesis.
I
would
Mathre,
while
and
like
to
of
on
my
in
Dr.
for
E.
L.
their
graduate
help
Dr.
and
committee
advice
and
the
my t h e s i s .
My a p p r e c i a t i o n
his help
thank
Dr . E . A. H o c k e t t
serving
preparation
for
and e x p r e s s
is
extended
to
doing experim ents
Dr.
Harold
arid w r i t i n g
Bockelman
my t h e s i s .
I w i s h t o e x p r e s s a v e r y s p e c i a l t h a n k s t o my f a m i l y
for
their
patience
I am v e r y
the
US
AID
University.
for
and
sacrifice.
grateful
to
the
sponsoring
my
Goverment
study
at
of
Turkey
Montana
and
State
to
my
vii
TABLE OF CONTENTS
Page
APPROVAL........................................................................................................................i i
STATMEN T OF PERMISSION TO USE.................................................... ; . . . i i i
DEDICATION.......................................
VI T A..........................
iv
v
ACKNOWLEDGEMENT......................................................................................
vi
TABLE OF CONTENTS............................................................................................. v i i
LI S T OF FI GURES.......................................
LI S T OF TABLES.......................................
%
xi
ABSTRACT.................................................................................................................. x i i i
Chapter
1
INTRODUCTION...................................................................................................I
2
LITERATURE REVIEW..................................................................................... 4
S y m p t o m s ........................................................................................................5
The B a c t e r i u m ......................................................
6
9
H o s t R a n g e ...............
E t i o l o g y a n d E p i d e m i o l o g y .........................................................11
S e l e c t i v e M e d i a .......................
' . . . I 1I
S c r e e n i n g f o r D i s e a s e R e s i s t a n c e ........................... . . . . 1 6
Me c h a n i s m o f R e s i s t a n c e .............................................................. 19
I n h e r i t a n c e o f R e s i s t a n c e ........................................................ 22
C o n t r o l ............................................... ......................................................2 1I
3
MAT ERI AL S AND
METHODS.................................................................26
M a t e r i a l s .................................................................................................. 26
I n o c u l a t i o n ............................................................................................. 29
D i s e a s e S c o r i n g ....................
32
S t a t i s t i c a l . P r o c e d u r e s , . . . . ................................................... 33
H
R E S U L T S ..............................................................
....35
viii
TABLE OF CONTEMTS-Cont i nuf i r i
Page
D i a l l e l S e t ............................................................................................ ..
R e s i s t a n t x R e s i s t a n t C r o s s e s .......................................35
S u s c e p t i b l e x S u s c e p t i b l e C r o s s e s .............................35
R e s i s t a n t x S u s c e p t i b l e C r o s s e s .......................... „ 35
CM 6 7 C r o s s e s ....................................................
35
H e r t a x CM 6 7 ............................
36
Summi t x CM 6 ? .................................................... 3 g
O d e r b r u c k e r x CM 67 . . . . ............................. 3 g
B e t z e s x CM 6 7 ........................................................2)1
SW I 91 C r o s s e s ..............................................................Ijl
H e r t a x SW I9 1 ........................................................2j 1
Summi t x SW I 9 1 ..................................................... 2|i
O d e r b r u c k e r x SW 1 9 1 ........................................ Jj Jj
B e t z e s x SW 1 9 1 .....................................................JjJj
R e s i s t a n t x S u s c e p t i b l e C r o s s e s ...........................................Jjg
CM 67 C r o s s e s ..................... .............................. ■....................jjb
Cl 1 2 5 5 8 x CM 67 .................................................. ! ! ] 1)6
Cl 1 2777 x CM 6 7 ........................................................... 1)6
Cl 1 2 86 6 x CM 6 7 .................................................
1)9
SW I 91 C r o s s e s ............................................................................ 9
Cl 1 27 87 x SW I 9 1 .................................................. ! ] Jig
Cl 1 3095 x SW 1 9 1 . ...................................................... 1)9
PI 38251 1 x SW I 9 1 ......................................................5 1)
PI 3826 50 x SW I 9 1 ................................................. .51)
PI 3 8 2 7 3 2 x SW I 9 1 ...........'........................................ 5 H
PI 3 8 3 0 7 7 x SW I 9 1 ......................................................55
K a n g b o r i C r o s s e s ......................................................................55
A l p i n e x K a n g b o r i .........................................................55
L u t h e r x K a n g b o r i .........................................................57
Cl 1 2 56 9 x K a n g b o r i ..................................
57
Cl 1 2 5 7 7 x K a n g b o r i ................................................... 57
Cl 1 2595 x K a n g b o r i ................................................... 60
Cl 1 2776 x K a n g b o r i ...............................
60
Cl 1 2777 x K a n g b o r i ................................................... 60
Cl 1 2866 x K a n g b o r i ................................................... 60
PI 3 8 2 7 2 0 x K a n g b o r i ................................................ 62
R e s i s t a n t x R e s i s t a n t C r o s s e s ............................
62
R e l a t i o n b e t w e e n E a r l i n e s s a n d S u s c e p t i b i l i t y . . 63
5
DI SCUSSI ON.......................................
65
D i s e a s e D e v e l o p m e n t a nd P l a n t i n g D e s i g n . . . . . . . . 6 5
E a r l i n e s s a n d S u s c e p t i b i l i t y ........................................ . . . 6 6
I n h e r i t a n c e o f R e s i s t a n c e ........................................................ 68
ix
TABLE OF CONTENTS-C o n t l n u e d
Page
The Use o f
6
Resistance
S o u r c e s ............................................73
SUMMARY ......................................................................................................... 75
LITERATURE CI TED................................................................................................. ..
X
LI S T OF FIGURES
Figure
I.
II.
III.
I V.
Page
P l a n t i n g d e si g n of f i e l d t e s t , H o r t i c u l t u r e
F a r m , B o z e m a n , 1 9 8 4 ...............................................................
31
F2 d i s t r i b u t i o n o f CM 67 a n d SW I 91 c r o s s e s
i n t h e d i a l l e l s e t ........................ .......................................
45
Fp d i s t r i b u t i o n o f CM 67 a n d SW I 91 c r o s s e s
i n t h e r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y . . . . 53
Fp d i s t r i b u t i o n o f K a n g b o r i c r o s s e s i n t h e
r e s i s t a n t x su sc e p tib le cross c a t e g o r y . . . .
xi
LI S T OF TABLES
Tables
Page
I . The f o r m s p e c i e s o f X a n t h o m o n a s c a m p e s t r i s
p v . . t r a n s l u o e n s a n d t h e i r h o s t s .................................................. 8
2.
B a r l e y c u l t i v a r s used as p a r e n t s i n t h e
p r o g r a m ............................................................................
crossing
27
3•
C r o s s e s made f o r t h e d i a l l e l s e t , a n d t h e i r p a r e n t s ,
F s a n d Fg s w h i c h w e r e e v a l u a t e d ......................................... 28
4.
C r o s s e s made i n t h e r e s i s t a n t x s u s c e p t i b l e and
r e s i s t a n t x r e s i s t a n t c a t a g o r i e s , and t h e i r p a r e n t s ,
F 1 s a n d FgS w h i c h w e r e e v a l u a t e d ....................................... ,..BO
5.
Disease
reactions
of
parents
in
the
diallel
s e t . . 36
6 . D i s e a s e r e a c t i o n s o f F 1 s a n d FgS f o r t h e
r e s i s t a n t x r e s i s t a n t and s u s c e p t i b l e x
susceptible
c r o s s e s i*n t h e d i a l l e l s e t ............................. 37
. 7.
D i s e a s e r e a c t i o n s of
CM 67 c r o s s e s i n t h e
p a r e n t s , F 1s a n d F2 s f o r
d i a l l e l s e t ......................................... 3 9
8.
P r o b a b l e F 1 g e n o t y p e s and h y p o t h e t i c a l
s e g r e g a t i o n s i n Fg S o f CM 67 c r o s s e s i n t h e
d i a l l e l s e t ................................... .............................................................HO
9.
Disease
crosses
r e a c t i o n s o f F 1s a n d FgS f o r SW I 91
i n t h e d i a l l e l s e t .............................................................. H2
10.
P r o b a b l e F1 g e h o t y p e s and h y p o t h e t i c a l
s e g r e g a t i o n s i n FgS o f SW 191 c r o s s e s i n t h e
d i a l l e l s e t . . .............................. ................................ ............................i|3
11.
D i s e a s e r e a c t i o n s o f p a r e n t s , F 1s a n d FgS f o r
CM 67 c r o s s e s i n t h e r e s i s t a n t x s u s c e p t i b l e
c r o s s c a t e g o r y ..................................
H7
I
12.
P r o b a b l e F1 g e n o t y p e s and h y p o t h e t i c a l
s e g r e g a t i o n s i n F2 o f CM 6 7 c r o s s e s i n t h e
r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y ............................HS
xii
Tables
Page
I 3 • H o m o g e n e i t y t e s t f o r SW 191 c r o s s e s i n
t h e r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y . . ....... 50
I A . D i s e a s e r e a c t i o n s o f p a r e n t s , F 1s a n d F2 S f o r
SW I 91 c r o s s e s i n t h e r e s i s t a n t x s u s c e p t i b l e
c r o s s c a t e g o r y ........................................................................................51
15.
P r o b a b l e F 1 g e n o t y p e s and h y p o t h e t i c a l
s e g r e g a t i o n s i n F g s o f Sw 191 c r o s s e s i n t h e
r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y . . . ! ..............52
16.
Homogeneity t e s t f o r Kangbori c r o s s e s i n t h e
r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y .........................5b
17•
D i s e a s e r e a c t i o n s o f p a r e n t s , F 1 s a nd F g s f o r
Kangbori c r o s s e s in the r e s i s t a n t x s u s c e p t i b l e
c r o s s c a t e g o r y ........................................................................................ . 5 8
18.
P r o b a b l e F 1 g e n o t y p e s a nd h y p o h e t i c a l
s e g r e g a t i o n s i n FgS of Kangbori c r o s s e s i n the
r e s i s t a n t x s u s c e p t i b l e c r o s s c a t e g o r y .........................59
19.
D i s e a s e r e a c t i o n s o f p a r e n t s , F 1 s a nd FgS f o r
the c ro sse s in the r e s i s t a n t x r e s i s t a n t cross
c a t e g o r y ................ .........................................................................................6 3
20.
C l a s s f r e q u e n c i e s a nd p e r c e n t a g e s o f e a r l y p l a n t s
i n t h e I 4 Fg p o p u l a t i o n s w h i c h h a v e a l a t e , r e s i s t a n t
p a r e n t and an e a r l y , s u s c e p t i b l e
p a r e n t ............... 6 4
xiii
ABSTRACT
I n h e r i t a n c e of r e s i s t a n c e t o b a c t e r i a l l e a f s t r e a k
wa s i n v e s t i g a t e d i n 23 b a r l e y c u l t i v a r s . P a r e n t s , F ^ s and
F qS o f one c o m p l e t e d i a l i e l s e t w i t h s i x v a r i e t i e s and
t h o s e o f 23 o t h e r c r o s s e s w e r e t e s t e d w i t h o n e M o n t a n a
i s o l a t e ( X- 6 7) o f X a n t h o mo n a s c a m n e s t r i s pv. t r a n s l u c e n s
i n t h e f i e l d . An i n o c u l a t i o n m e t h o d i s d e s c r i b e d w h i c h
r e s u l t i n a u n i f o r m l e v e l of i n f e c t i o n .
B arley c u l t i v a r s , H erta, Summit, O d erb ru ck er,
B e t z e s , A l p i n e , L u t h e r , Cl 1 2 5 5 8 , Cl 1 2 5 6 9 , Cl 1 2 5 9 5 , Cl
1 2 7 7 7 , C l 1 2 7 8 7 , C l 1 2 8 6 6 , Cl 1 3 0 9 5 , P I 3 8 2 5 1 1 , P I
3 8 2 6 5 0 , PI 3 8 2 7 2 0 , PI 3 8 2 7 3 2 , a n d PI 38 3 0 7 7 w e r e f o u n d t o
be p r o m i s i n g
s o u rc e s fo r r e s i s t a n c e to b a c t e r i a l l e a f
s tre a k . Resistance in these c u l t i v a r s varied with regard
t o g e n e a c t i o n a n d n u m b e r . So me o f t h e m may h a v e
identical
genes
or
differrent
genes in the
same
chrom osom es. F u r th e r study is needed to d e te rm in e
i d e n t i c a l , l i n k e d , and i n d e p e n d e n t g e n es . A ls o , a c l o s e
r e l a t i o n , w i c h s u g g e s t s a l i n k a g e , was f o u n d b e t w e e n
e a r l i n e s s and s u s c e p t i b i l i t y .
I
CHAPTER I
IHTRODOCTXOff
Bacterial
disease
pv.
caused
by
translucens
has in c r e a s e d
years,
and
mercuric
these
the
are
seed
irrigated
In
cereals
decreases
susceptible
treatm ents
available
treatm ents,
to
control
Breeding
control
for
diseases.
In
program,
breeders
reliable
screening
pathogens,
produce
resistance,
especially
genes
Review).
in
the
susceptible
Therefore,
disease.
the
method
of
has
been
mechanism
as
of
disease.
a
to
breeding
germplasm ,
with
and
a
other
can o v e r c o m e h o s t
resistance
backgrounds
combining
the
implement
B acteria,
the
curtailm ent
another
which
Organic
controlled
effective
ne w s t r a i n s
p a s t few
grown
resistant
test.
if
in
the
disease
barley v a rie tie s
this
is
camp e s t r i s
the
in
wide
(Hall
After
to
world
barley
transmission
order
need
fields
yields
to
resistance
a
Mont ana,
apparently
no
seed
is
X a n t h o mo n a s
Dow s o n .
f o r a number of y e a r s .
seed
single
cereals
bacterium,
(J.J.R.)
in
of
I 9 8 3 ) . Al l ' , c o m m e r c i a l
Montana
disease
streak
reportedly
and S a n d s ,
in
leaf
is
determined
(See
resistant
by
Literature
genes
from
I
2
different
sources
Expression
influenced
of
to
Literature
The
streak
small
infection
appropriate
has
For
the
screening
met hod
of
is
and.lines
that
the
c a n be
difficulty
in
(See
of f i e l d
the
to
variation
very
in
large
creating
tests
an
i s ^necessary.
bacterial
Previously
for
in
developing
field
resistance
screened
Plant
of s c r e e n i n g
reasons,
unknown.
were
results
is
ma y be s u s c e p t i b l e
results
above
streak
s a m e ( Ki m , I 9 8 2 ) .
cultivar
The
leaf
environment
the
field
made t h e
the
barley
varieties
the
area.
inheritance
in
not
a particular
a
unreliable.
by
ma n y c a s e s ,
in
strategy.
to b a c t e r i a l
I t has been observed
of
within
a breeding
extent
are
resistant
reaction
uniform
in
tests
the greenhouse.
even
great
Review),
cultivars
be
resistance
a
and g r e e n h o u s e
in
should
some
disease
leaf
barley
resistance
a n d s ome o f t h e m w e r e f o u n d t o be p r o m i s i n g a s s o u r c e s o f
resistance
this
study
resistance
reliable
of
(Stewart,
were
to
1 9 5 2;
to
determ ine
bacterial
screening
resistance,
leaf
techniques,
and
to
resistant
barley
streak.
is
that
hoped
I 98 2) .
the
streak
to
devise
developing
It
a n d Ki m,
a
varieties
inheritance
in
find
The g o a l s o f
barley
by u s i n g
different
breeding
to
a long-lasting
of
sources
plan
for
bacterial
leaf
resistance
to
3
bacterial
combining
leaf
streak
resistance
in
from
barley
various
might
be
sources.
developed
by
CHfiPTEB 2
LITERfiTDRE RBFIEH
B acterial
bacterium,
leaf
streak
Xanthomonas
The
c a me f r o m
an
unusual
barley
leaf
a nd
This
( 1 917).
earliest
Madison,
Colorado,
Dakota,
reported
Iowa,
Oregon,
(Pady,
numerous
1981;
in
Miyajima,
sprinkler
within
the
wide
1982).
and
The
irrigated
past
leaf
leaf
1946;
disease
barley
few y e a r s
by
North
of
e,t
barley
Dakota,
Europe
streak is
rye,
Koleva,.
1 9 82 ;
has
and
aI .
in
South
triticale,
1981;
Mathre,
become
and S a n d s ,
Asia
now k n o w n t o
and
Leyns e t
1 9 82;
prevalent
and w h eat f i e l d s
(Hall
two-row
Jones
streak
wheat,
Schmidt,
a p p e a r e d as
I t was f ound i n N e b ra s k a
N orthern
(W allin,
barley
other v a rie tie s.
Mont ana,
Bacterial
(J.J.R.)
on
Montana
described
bacterial
on b a r l e y ,
grasses
Egli
first
disease
of
the
1 8 OOs ( M a t h r e , .
1912 w h e r e i t
to
by
translucens
this
plot
and W i s c o n s i n .
1944),
occur w o r ld
a
spread
Minnesota,
( J a c z e w s k i , I 93 5 ) .
a I .,
was
in
pv.
caused
the la t e
of
Wisconsin in
subsequently
The y
since
report
blight
disease
grasses
cam n e s t r i s
Dawson, has been o b s e r v e d
1982).
of
of
1983).
and
in
Montana
5
Early
reports
epiphytotics
(Dickson,
on
reduces
Sands,
I 983).
fields
has
1968)
Yield
by
reduction
to
and
general
reduced
bacterial
10-15%
estimated
local
cultivars
Commonly,
yield
been
that
susceptible
I 956).
barley
showed
leaf
streak
( M a t h r e , 1 9 8 2;
of
be
severely
as
high
Hall
infected
as
yield
in
and
wheat
50% ( H a g b o r g ,
.
S ffP P tO jG L S
The
green
first
leaf
lesions
streaks
blade
that
regions.
symptoms
later
between
leaf
t r a n s i ucency
this
then
droplets
characteristic
barley
In
the
young
water-soaked
and
dark-brown
of
stage
of
characteristic
conditions,
leaf
appearance
in
distinguishing
1 9 8 2 ). U n d e r d r y c o n d i t i o n s
a
length
Un d e r
as numerous
and b a r l e y
later
narrow
exudate
lesions.
the
into
A bacterial
The
stripe,
the
the e n t i r e
show
I 9 5 6 ).
the
giving
on
coalesce
extending
lesions
may a p p e a r
appearance.
blotch,
on
small,
light-brown
veins,
(Dickson,
present
exudate
yellow
as
( Z i l i n s k y f I 983).
the
appear
t e n d to d e v e l o p as l o n g i t u d i n a l
stripes
developm ent,
usually
become
the
barley
sheath
These l e s i o n s
glossy-surfaced
the
and
on
humi d
tiny
cream-like
surface
of
a
stripe
to
shellacked
exudate
this
is
is
disease
mosaic
a
key
from net
( Mathre,
the exudate q u ick ly hardens
6
into
yellow
detached
(Jones
granular
and
readily
e ta l.,
Similar
termed
to
results
spike
and
lesions
dark
in
retarded
be s e e n
of
or
scales
dissolved
d e v e l o p on t h e
Severe
spike
elongation
tissues.
easily
in
shellac
on t h e
grain
bracts
water
can
and a r e
turn
infection
of
the
h e a d may be b e n t
Bacterial
surface
ma y be b l i g h t e d
light
usually
a nd b l i g h t i n g
An i n f e c t e d
I 956 ) .
the
head
late
(Dickson,
as
floral
The e n t i r e
brown.
distorted
a portion
softened
chaff".
and a d j a c e n t
often
or g l i s t e n i n g
1 9 1 7 ).
' ’b l a c k
very
beads
or
growth
the
(Hall
can
seeds
and
and Sands,
I 983 ) .
El-Banoby
persistent
from
Rudolph
water-soaked
susceptible
with
and
cultivars
preparations
of
of
(1979)
leaf
spots
barley
were
and w h e a t
extracellular
X s-Ulksms Jia.s f i s m s s s l s l s
reported
p
that
induced
in
by t r e a t m e n t
polysaccharides
(ESP)
v . .I s s fis lfif ie ns
f.sp.
cerea lis.
Tkie B a e t e p i u a
-XfifiikfifflfiHSS
Dow s o n ,
the
causal
fififflfifisin is
organism
pv.
t r a n s l u c e ns
or b a c t e r i a l
leaf
b a r l e y , b e l o n g s t o t h e g e n u s -XSfilkfifflfifiSS*
Dye. (1 9 8 0 ) ,
the
Gr am n e g a t i v e
genus
rods
Xanthomonas
O.if x 1. 0
urn,
is
s t r e a k of
A c co rd in g to
defined
single
(J.J.R.)
polar
as
follows:
flagellum,
7
aerobic,
catalase
negative,
Twe e n
indole
at
not
present
found
are
All
plant
in
association
polysaccharide
YDC a g a r
The
and
differentiated
the
from
of
the
bacteria
tests
i r a n s l u c e ns can n o t
by i t s
in
(Dye,
1980).
et
al.,
Fang
et
al.,
Hagborg,
X. c .
their
et
pv.
1971;
al.
1942;
Dye,
I 9 84).
t r a n s l u c e ns
host
specifity
containing
agar
or
al b il i ne a ns ,
JL-
positive
1 980; E g l i
Previously,
have
been
(Table
I).
be
test
for
nomenspecies
can
and by
camo e s t r i s
and i t s
1919;
oats,
Reddy
1950;
and S c h m i d t ,
form
described
pv.
strains
triticale,
eight
can
on SX a g a r
JL.
g r o w on SX a g a r
grasses
material.
are
characteristics
(Smith
Leyns
plant
are
X a n t h o mo n a s
this
and
Shekhaw a t ,
known,
e x tra c e llu la r
genus
rye,
1924;
as
on n u t r i e n t
p a th o g e n ic to b a r l e y , w heat,
other
recognized
JL. f l a s i e s i f l i s
the o th e rs
The
a nd
and s h i n i n g .
JL. -S-HJle l i n s .
by g r o w t h
pathogenicity
s o me
or
f ra & a rla g .,
digestion.
be i d e n t i f i e d
plants
oxidase
produced,
species
so f a r
species
convex,
n a .m £ S .S lZ iS .,
protein
and,
with
these
n o me n s pe c i e s
a JCS-JIflJDSlJELi s ,
X a n t h o mo n a s
produce
of
mucoid,
five
not
s l i m e " g u m - x a n t h a n " on m e d i a
Colonies
are
positive,
nitrate
pathogens
xanthom onads
glucose.
H2 S
80 h y d r o l y s i s ,
produced.
only
Most
positive,
are
rice
et
al.,
Patel
and
1 982 ; a n d
species
of
according
to
8
Table
I.
The f o r m s p e c i e s o f X a n t h o m o n a s c a m p e s t r i s
t r a n s l u c e n s and t h e i r h o s t s .
Form s p e c i e s
Hosts
References
JCct f . s p .
undulosa
wheat, s p e l t ,
b a r l e y and
rye
Smith,Jones
1919.
Xc t f . s p .
secalis
rye
R e d d y , G o d k i n a nd
J o h n s o n , I 924.
Xc t f . s p .
horde!
barley
r i ce
a nd
Hagborg,!942;Patel
a n d S h e k h a w a t , ! 97 I .
Xc t f . s p .
hordeiavenae
barley
oats
a nd
H a g b o r g , 1942.
and
Reddy,
Xc t f . s p .
cerealls
wheat,oats,
H a g b o r g , ! 9 4 2 ; Fang
b a r l e y , rye
e t a l . , 1 9 5 0 ; E g l i and
s m o o t h br ome
S c h m i t , I 982 .
grass,quack grass,
I t a l i a n rye g r a s s ,
p e r e n n i a l rye g r a s s ,
a n d meadow f e s c u e
Xct f . s p .
ohlei
Phleum s o .
Xct f . s p .
-POa e
Poa
sp.
W a l l i n a n d Re d d y ,
I 94 5 ; E g l i and
Schm idt, 1982.
E g l i and S c h m i d t ,
1 982 .
Xc t f . s p .
Arrhenatherium
arrhenatheri
so.
E g l i and S c h m i d t ,
1982
X c t = Xanthomonas
pv.
campestris
translucens
pv.
9
flost Range
According
pathogens
seasons
to S c h u s te r
with
on
wide
alternate
off-seasons.
Such
discontinuous
plant
narrow
host
host
growth
disease
rye.
Previous
in
the
grass,
show
f.
shows
s p.
that
by
have
orchard
sp.,
grass,
Italian
( Smith
1 942;
1950;
B o o s a l i s , 1 952;
Cunfer
on
oats,
importance
the
of
JCant , hoff l onas
Wallin
Patel
barley,
barley,
brome,
water
m ille t,
fescue
of
cereal is
to wheat,
the
that
include,
foxtail
grass
Ha g b o r g , .
I 98 1;
during
the overwintering
was p a t h o g e n i c
example
rice,
1 924;
al.,
crop
handicapped
parasites
translueens
These
Japanese
meadow
the
a bridge
p v . t r a n s l u e e n s g r o u p h a s 23 d i f f e r e n t
Ar r h e n g t h e r U f f l
and
not
between
from w i l d f l o r a .
smooth b ro m e , ch ea t
grass,
It
studies
triticale,
quack
are
unlike
pv.
This
Gr a m i n e a e .
oats,
provide
investigated
transmission
Gampestris
survive
ranges.
quack grass.
and
can
which
pathogens
JCanthefflQnas c a s e e s i r i s
barley
C o y n e ( 1 9 7 H) , b a c t e r i a l
ranges
hosts
B o o s a l i s '( I 9 5 2 )
infected
and
rye-grass,
et
and
a I .,
Re ddy,
and S h e k h a w a t ,
and S c o l a r i ,
1982;
Reddy
1 945;
Egli
canary
Poa
perennial
1919?
grass,
reed
sp.,
rye,
einkorn,
bristle
foxtail,
Phleum
wheat,
spelt,
yellow
hosts
sp.,
rye-grass
et
al.,
Fang e t . a l . ,
I 9 7 1 ? Leyns
et
and S c h m id t,
1 9 82;
Ki m,
1982;
Barley
species
( 1 9 81)
seems
of
of
&*. 1L»- p v .
the
cereal
Cunfer
fields
a nd
to
triticale,
barley.
They r e p o r t e d
species
wa s
in
range,
host
The
form
be p a t h o g e n i c
Patel
and
old
being
and
one
from
pathogenic
barley,
found
rye,
on t h e
only
host
only
barley
(Hagborg,
t o L l SL>. p v . ^
stages.
pv.
f.sp.cerea l i s
grass,
quack, g r a s s ,
occurs
and
to
strains
were
equally
of
were
to
virulent
on g r a s s e s .
Bamberg
(1936)
translucens
differ
in
found
which
they
each
host
reported
that
the
rice
( 1950),
naturally
on
smooth
that
pathogenicity.
strains
of
was
20 a n d
al.
water-soaked
to
However,
Fang e t
produces
rye
barley.
s y m p t o m s on b a r l e y f o l l o w i n g wo u n d i n o c u l a t i o n ,
mo r e
and
to
restricted
1 9 42).
f . s p . io rid .e i a t
According
a nd
that
originally
showed
wheat
wheat
primarily
wa s
al.
pathogenic
from
barley
et
mu c h l e s s
cultivar
horde!
(1971)
but
from
species
to
Hall
tritlcale
strains
Strains
S h e k h a w. a t
susceptible
day
that
however,
tested.
(1982)
wheat
I).
Mont ana we r e
from
most v i r u l e n t
were i s o l a t e d ,
from
of
Scolari
to most of the form
(Table
isolates
i.r a .a a lj l& e .n a .
usually
1984).
tra n slu c ens
virulent
were
al.
be s u s c e p t i b l e
that
rye in i r r i g a t e d
barley.
to
pv.
reported
on
and Leyns e t
40
JL. Cj .
brome
streaking
but i t
is
L l G-l P v .
According to
Hagborg
(I 9 4 2 ) ,
o.
different
pv .
isolates
t. r s . JlS lJlS fi. HS
capablities
and
races
this
within
he
of
the
are
different
suggested
special
s a me f o r m
the
need
species
o f JLu
in
pathogenic
for
recognizing
for m.
Etiology and Epidemiology
Bacterial
affecting
infects
leaf
leaves,
leaves
bacterial
parenchyma
leaf
(Jones
invasion
of
leaf,
parenchyma
of
the
leaves
no
infected
et
a I .,
is
glumes.
and
bacterium
spreading
1917 and B a m b e r g ,
chlorenchyma
sheath.
and
The
wounds,
confined
^bundle
( Sheakhavet
occurlng disease
to
the
in tercellu lar
leaf
vascular
and
stomata
possessing
mesophyll
a widely
sheaths,
through
i n t e r c e 11u l a rIy
The
streak is
ground
naturally
elements
Patel,
thin-walled
spaces,
and
In
I 936 ) .
were
i.e.,
tissue
infected
shown
to
be
1 97 8 ).
Th e s e e d - b o r n n a t u r e o f t h i s d i s e a s e w a s r e p o r t e d by
Jones et
a l . ( I 9 I 6 ) and Sm ith
penetrates
plumula
infected
pericarp
through
Spreading
reaches
the
wounds
rapidly
by
or
primary l e a f
develops
(Wallen,
According
to
a l . ( I 919).
causing
stomata
through these
the en clo sed f o l i a g e
leaf
et
The b a c t e r i u m
infection
on
the
tissues,
leaves.
of
coleoptils*
it
finally
By e l o n g a t i o n ,
the w ater-so ak ed
tne
sureaks
the
on t h e
1946).
Boosalis
(1952),
barley
plants
from
infected
seeds
planted
percentage
of
rionster i l i z e d
soil.
and
rye
a few
seedlings
fungus
to
from
He f o u n d
with
that
bacterium
ma y
seeds
whereas
barley,
alone
to
both
a higher
planted
of
25
co-inoculated
Other
than
persist
from
one
seed
wheat
in
HO p e r c e n t
of
with
a root
rot
succumbed
transmission,
season
s ome o t h e r
in
resulted
a n d Xl t r a n s l u c e n s
streak.
of b a r l e y , w h e a t ,
s howed
those
Xl t r a n s l u o e n s
seedlings,
seeds
soil
than
(H e l m i n t h o s n o r i u m sp.)
Xanthomonas
straw
sterilized
in fe c tio n
inoculated
infected
in
to
grasses,
the
this
next
on
a n d on w i n t e r
hosts.
H ed r ic k( '1 956)
bacterial
high
exudates
waterholding
during
unfavorable
S c h u s t.e r
and
conditions
and
Leach
capacity
Coyne
commonly f a v o r s
to
in
The
bacteria
from
antagonistic
c.
pv.
for
on o r
bacterial
movement .
t r a n s l ucens is
Jones et
aid
and
(1974),
favorable
moisture
may
conditions
Residues
protected
a l . ( 1 957)
thought
behave as a h y d r o p h i l i c
residues.
soil.
et
the
survival
in
dry,
a I . ( I 9 T7 ) r e p o r t e d
undecayed
for
tolerant
that
in
surface
those
microflora
Probably
very
t^an
under
survival
soil
to
dry
plant
a r e more
residues
may
above
dry
to
incorporated
which
the
Its
survival
According
m aintenance
bacterial
near
colloid.
bacterial
seasons.
that
are
require
reason,
Xl
conditions..
the bacterium
survived
13
for
eight
years
m o n t h s on s t r a w
on
seeds.
from
According
to
blighted
Boosalis
plants
( 1952),
C and i n
the
soil
the
was s t e r i l e
( 1936) re p o rte d
dry
field
soil
at
organism
ranging
can
to
and
that
St.
during
the
Paul,
C,
winter
bacterium
months
He
extremely
remaining
at
unless
Bamberg
s u r v i v e d 77 d a y s
Minnesota.
at
pv.
kept
a s e p s i s was m a i n t a i n e d .
survive
-33°
the
two
JL.
was not a b l e to s u r v i v e l o n g i n s o i l
27°
and
viable
found
low
in
that
in
this
temperatures
soil
cultures
for
a t l e a s t I 2H d a y s a f t e r D e c e m b e r I 5.
Bamberg
retarded
( I 936 )
the
found
growth
retarding
effect
hum idity
and
of
was
became
being
Severe
below
temperature
Bamberg
( 1 9 3 6 ),
20°
as
of
the
incubation,
occur
around
R. H.
of t h i s
40° C w i t h
two
to
at
in
had
period
seven
I 0°
wet
The
relative
decreased.
organism
on
for
t h e mi n i mu m
seasons
2 0 0 C ( K i m , 1 9 82) .
temperature
while
50 p e r c e n t
the
growth
culture.
C. The m a x i m u m t e m p e r a t u r e
incubation
C from
in
humidity
1 0 ° C.
epidemics
optimum
At
the
at
g r o w t h was a p p r o x i m a t e l y
slightly
length
for
relative
bacterium
greater
between 25-30°
sustained
the
low
was n o t i c e a b l e
Optimum t e m p e r a t u r e
agar
that
with
According, to
a marked e f f e c t
and
days
C from
disease
were
eight
on t h e
development.
necessary
to
the
20
days
for
were
required.
below
Disease
10°
C.
infection
in
appear
Under
and
the
1.8°
( 1936)
under
2 7 ° C,
by
15.5°
C day
and
that
humidity
is
that
occurred
to
Kim
C night,
more o f t e n
4 .5 °
15.5 t o
I 80
a t 2 110
for
symptom
S y mp t o ms
C night
and
did
regime.
32°
developed.
C day
Bamberg
developm ent,
a lim iting
or
highest
(1982),
12.8°
disease
at
temperature
and
for
the
at
temperature.
symptoms
mo r e
infection
C day
regimes,
reported
even
an o p t i m u m
According
the
21.1°
reported
plants
influenced
C night
relative
low
was
slowed
a t 2 1 ° C5 s l i g h t
at
culture.
development
was
( 1.9 5 2 )
infection
a n d no i n f e c t i o n
growth
not
Stewart
on s u s c e p t i b l e
C, m o d e r a t e
C,
development
factor
low
than
temperature.
Effective
aphids,
wind,
occurs
only
I 952).
Field
marked
rain
wh e n
and
the
that
meters
of
from
by d i r e c t
host
is
epidemiology
strain
indicated
.. s q u a r e
transm ission
JL*.
plant
this
bacterium
from
a single
to
to
in
f.
capable
infection
of
(Boosalis,
s p.
using
a
h o.£ de. i
spreading
locus
by
contact,
Montana
.tr a D a liL g ^ n s .
is
plant
plant
water-congested
studies
pv
plant
within
28
39
d a y s ( H a l l e t a l , 19 8 1 ) .
Selective Media
Selective
different
media
xanthomonads
that
are
have
not
been
efficient
developed
for
for
isolating
15
Xj. g a mjDe s t'jr I
agar,
not
p'v. t r a n s l u c e n s
s
selective
for is o la tio n
K M- I
Chemical
K2 KPOjj
This
St.
( Difco
(Mallinckrof t
Bacto
agar
a hot
plate
with
I
the
tobramycin
and
( 1 : 1,
v/v)
with
and
I
Inc.,
to
yg/ml,
final
bacterium.
medium,
but
(Sigma),
of
a sensitive
Other
have
not
been
15 g o f
Before
on
t o 6. 6
autoclaving
these
in ethanol,
ethanol-w ater
of
of
and r e l i a b l e
spp.
in
hydroxide
are
100 y g / m l ,
(1982)
(1:1,
ethanol-water
Kentucky)
found
NHjjCl
adjusted
sodium
%a n t h o m o n g s
of
completely
pellet
Ki m
yeast
water.
in
concentration
(Sigma
0.8 g o f
MO.) a n d
dissolved
I
pv.
g of
g
dissolved
in
Paris,
respectively.
me d i u m p r o v i d e s
pH i s
After
(Sigma),
I
dissolved
and
the
trehalose
0. 03
distelled
dissolved
addition
(M allinckroft
aseptically
bar
cycloheximide
ampicillin
D( + )
(Sigma),
Louis,
are
solution.
(Sigma),
g of
acid
St.
double
stirring
NaOH
ingredients,
of
lactose
D etroit),
Wo r k s ,
used
ear n ^ e s t r i s
respectively,
ingredients
with
N
v/v),
liter
generally
1.0 g o f
thiobarbituric
Chemical
Xj .
4.0
Laboratories,
per
adding agar,
of
MO. ) ,
KH2 POjj ( S i g m a )
is
W i l b r i n k 1s
Ki m ( 1 9 8 2 ) d e v e l o p e d
contains
Louis,
I 9 8 2 )..
bacterium,
isolation
me d i u m
0.2 g of
and
extract
for
Co . ,
(Sigma),
the
and m a i n t e n a n c e .
medium
translufiens.
for
(Kim,
noted
added
8 i j g / ml
that
the
d e t e c t i o n of the
grow
on
cereal
the
KM- I
grains.
He
O
16
also
added t h a t
soil-born
plant
Schaad
strains
of
for
and
whe n
qg
of
contains
of
Xj. S j . p v .
Idaho
of
the
against
10 0
agar,
qg
in one l i t e r .
that
grew
from
seeds
g r o w on XTS a g a r .
from
seeds.
XTS
5 g of g lu c o s e ,
200
They r e p o r t e d
associated
p o o r l y on
bacterium
gentamycin,
bacteria
many
M e d i u m , XTS a g a r ,
t r a n s l u s e ns
23 g o f n u t r i e n t
not
from
isolation
saprophytic
did
reported
a semiselective
cycloheximide,
cephalexin
(1984)
translucens
They d e v e l o p e d
selectivity
bacteria.
Forster
used fo r
isolation
agar
me d i u m h a d h i g h
pathogenic
Xt Ci. p v.
KM- I a g a r
seeds.
this
with
and
8
i}g o f
that
91 % o f t h e
wheat
and b a r l e y
S c r e e n in g f o r D ig e ag g R e s is ta n c e
Most
of
resistance
the
early
to
bacterial
locations
where
natural
necessary
to
a
uniform
necessary
can
be
inoculate
disease
so
I.
1 917)
the
barley
Spraying
epidemics
test
different
plants
following
with
bacterial
select
were
for
tecniques
Gt
pv.
in
it
is
to obtain
I 97 8 ) .
lines
for
out
However,
artificially
breeding
Xt
plants
carried
occur.
(Russell,
compared
plants
to
diseases
epidemic
accurately
Historically,
inoculate
that
attempts
This
and
is
genotypes
disease
reaction.
have
used
been
to
t ranslucens:
suspension
(Jones
et
a l .,
17
2.
Partial
vacuum t e c h i q u e
( B o o s a l i s , 1 950 ) .
3. I n j e c t i o n o f b a c t e r i a l
syringe
( B a m b e r g , 1936;
ii.
Seed
suspension
5.
a
Seedling
sharp
6.
evening,
off
followed
suspension,
and
top
poking
the
flooding
of
the
by i m m e d i a t e
suggested
Injecting
into
his
the
the
seedling
with
barley
with
bacterial
plants
spraying with
irrigation
method
at
in
the
bacterial
a 3 da y
interval
sheath
found
studies
that
and d i f f e r e n t
Oderbrucker
53 t e s t e d
the
( # 3 )i
the
into
of
most e f f e c t i v e
the
an
partial
leaf
older
of
methods
a seedling
plant
with
vacuum t e c h n i q u e
a
( # 2 ),
( # 6 ).
sources in barley
(1917)
that
inoculum
leaf
Previous
that
bacterial
1936).
the
hypodermic syringe
of
in
1982).
were:
and
seed
1946).
by
and
sprinkler
Kim ( 1 9 8 2 )
or
soaking
(Wallin,
needle
(Hagborg,
Mowi ng
by
inoculation
nichrome
suspension
( Ki m,
one h o u r
by h y p o d e r m i c
and H a g b o r g , 1 9 3 6 ) .
inoculation
for
suspension
revealed
that
there
to b a c t e r i a l
leaf
streak.
Chevalier,
from
(Cl .
4666)
barley
barley
the
California,
cultivar
were
the
cultivars.
cultivars,
Spartan,
Jones et aI .
released)
resistant
Stewart
resistant
Summit(six-rowed
recently
most
are
( I 9 5 2)
Cl 6 2 4 0 ,
and
cultivars.
reported,
Velvon,
a nd
s ome o t h e r
Patel
lines
and
showed hi gh
Shekhawat
the s e e d lin g stage
f .
s p. k oZ iiS i.
variations
in
the
to
degree
and
21
leaf
Barley
Screening
lines,
tests
for
of f i e l d
showed
between
field
that
the
that
and
leaf
resistant
infected
wh e n
the
that
field,
but
but
varieties,
for
and
resistance
He r t a ,
Luther,
Be t z e s ,
resistant.
He a l s o
from
Ethiopia
in
the
carried
out
the
barley
were
reflect
the
more a c c u r a t e l y
than
( R u s s e l l , I 97 8 ) . P r e v i o u s
is
usually
tests
on c e r e a l s .
in
diseases
generally
tests
field,
susceptible
correlation
resistance
Bamberg (1936)
Mi n d u m
yet
were
inoculated.
varieties
no
for
Marquis,
hypodermically
s ome
be
bacterial
greenhouse
varieties,
appeared
noted
to
mostly
there
streak
wheat
in
observed.
varieties,
Alpine,
resistance
g re e n h o u se or l a b o r a t o r y
bacterial
Barley
conditions
studies
were
Collection
found
eultivars
resistance,
54 commercial
were
resistance.
Collection.
natural
effectiveness
barley
susceptiblity
Oderbrucker,
Shabet
51
complete
streak.
resistant
USDA W o r l d
under
no
of
screened
S u m m i t ( MT 72 9 ) ,
found
found
of f i e l d
t o %«_ Cj . P v . t.Z S n s l j n c pS.HS
f r o m t h e Wor l d B a r l e y
bacterial
Wa be t ,
tested
for reaction
They
Ki m ( 1 9 8 2 )
722 l i n e s
(1971)
degrees
were
in
reported
and
Kubanka
rather
heavily
Stewart
quite
the
to
(1952)
resistant
greenhouse.
in
Kim
19
( 1982) did not f in d
results
in
the
any s i g n i f i c a n t
growth
chamber
a nd t h e
MecfoaaJtsra o f
The
bacterial
leaf
two t y p e s
(i)
streak
Preformed
inhibit
bacterial
the
plant
their
(stom ata
or
suggested
that
surface
controlled
the
the
to
intercellular
are
able
though
the
to
the
host
as t h e i r
plant,
bacterial
to
of
bacteria
enter
on t h e
the
al.
the
the
contains,
for
. wh e n
et
of
genetically
influence
most
(1970)
host
fluid
in
host
is.
z itx o .
specific
reported
plant,
in
abundance,
pathogenic
cultivated
p la n t only the h o st
Sasser
are
(1972),
plants
necessary
gr ow.
morphology
infection.
Element
bacteria,
living
ma y
(1978)
distribution
which
spaces
openings
Russell
and
which
b a^c t e r i a
natural
size
are
resistance.
intercellular
wounds.
tu
diseases:
mechanisms
through
or
there
Pathogenic
concetration,
spaces
nutrients
saprophytic
plants
as w e l l
induced
into
characteristics,
According
inside
host
lenticels)
susceptibility
all
penetration
or l e n t i c e l s
of
(ii)
involves
barley
to b a c t e r i a l
( E l e m e n t , 1 972).
penetrate
stomata
and
in
Generally,
mechanisms
resistance
field.
resistance
unknown.
resistance,
between
R e sista n c e
of
is
of r e s i s t a n c e
Preformed
of
mechanism
correlation
the
and
But
bacteria
that
even
osmotic
20
potential
in.
controlling
factor
outside
normally
air
pathogenic
and
in tercellu lar
in
the
the
reduce
the
multiplication
fluids
a response
ma y
change
affects
to
within
effectiveness
He
also
affects
of e nzyme s
found
that
that
the
bacterial
S a n d s , 1 966;
In
and
to
includes
as a r e s u l t
induced
defense
diseases.
As
the
by
pH o f
plant
sap
penetration
and
bacterial
pathogens.
necessary
host
plant tissue
preformed
defense
of
for
the
tissues.
may i n h i b i t
Hildebrand
reaction
:
(i )
( I '9 6 7 ) ,
is
preimmunity
which
regarded
manifests
with
one
resistance,
mechanisms
infection.
According
(inoculated)
allow
bacterial
( G a r b e r , I 961;
hypersensitivity.
immunity
and
and
K l e m e n t ,1 9 7 2 ) .
contrast
resistance
plants
multiplication
humidity
of
nutrients
in
of
capacity
formation,
substances
The d r y
plant.
p a t h o g e n ma y be a b s e n t f r o m t h e r e s i s t a n t
Some a n t i b a c t e r i a l
a
buffering
to
produced
is
increase
relative
host
infection,
the
disease.
potential
the
resistance
fluid
population
osmotic
bacterial
and
of
A p e r i o d of h i g h
Garber ( 1961) suggested
plant
leaf
development
inhibits
bacteria.
rainfall
bacterial
the
There
that
are
start
in
t wo t y p e s
Preimmunity,
to
induced
(i i )
and
Go o d ma n
as a n o n s p e c i f i c
acquired
itself
bacterium
Klement
and
of
in
plants
that
pretreated
immunizes
or
21
protects
the
plant
from
bacterial
pathogen.
d iffe re n t
defense
preimmunity.
of
me cha ni s m
an
mechanisms
pathogenic
bacteria
host
die
race
Mew e t
orvzae
the
leaf
these
did
aI .
seems
release
reaction
particular
host
and
penetration
and
cavities,
this
of
a few
confines
practically
to
for
resistance
hypersensitive
remains
found
rice
multiplied
and
s ome
bacteria
inhibited
activity.
the
two
the
f r e e from
be a s s o c i a t e d
with
br eakdown.
(1984)
multiply
cell
bacteria
the, p l a n t
p o re s . However,
not
second
substomatal
on
s ugges te d.that
and
the
that
a short-lived
between
the
Hypersenstivity
specificity
pv.
into
another
e lic ite d
The
Following
around
so t h a t
the
reaction
genotypes.
symptoms.
by h o s t
by
noted
are
reflect
(1, 972) d e f i n e s
bacterial
infection
may
caused
incompatible
cells
(1980)
substances.
may be
El ement
as
Goodman
The f i r s t
antagonistic
postinfection
that
outside
the
entered
a strain
significantly
nonpathogenic
from
Xa n t h o mo n a s
that
the
bacteria
dividing
by
water
pores
leaves
lost
on t h e
c a mp e s t r i s
its
leaf
through
virulence,
surface.
were
excretions
of
They
immobilized
from
water
pores.
Ma n y
mechanisms
factors
of
are
resistance
involved
to
in
bacterial
the
complicated
diseases
in
plants
22
and
mu c h
research
mechanical
have
and
is
still
molecular
unique advantages
ability
to mu lt ip l y
strains,
and
thus,
processes
rapidly,
ove r c ome
JnherAtance
Inheritance
leaf
streak
failed
to
follows
is
find
Th e
no
about
diseases.
resistance
to
genetic
controlled
it
is
Th e r e s i s t a n c e
dominant
or
or
different
a recessive
nonspecific
Cu, I 97 3 5 E z u k a
and
by
( Co y n e
et
al.,
Chaudha r y , I 97 8 ;
Thes e
results
have
to
have
1 975;
Web s t e r
suggest
the
in
rice
indicated
that
be
a nd
Mu r t y
to
that
disease
to
and
conflicting
orvzae
others
Ya ma mo t o e t
that
bacterial
resistance
pv.
workers
et
diseases
reported
to the
a l . , I 97 I ;
search
to l o c a t i o n
of
characteristic
et
s o me
reached
control
while
bacterial
bacterial
c a mo e s t r i s
monogenically
reported
to
So me w o r k e r s
to
reference.
according
is
been
the
new v i r u l e n t
literature
Resistance
Xa n t h o mo n a s
polygenic.
or
authors
the
such as,
barley
A lengthy
considerably
Bacteria
resistance.
in
resistance
Different
conclusions
involved.
the
Resistance
citation
pattern.
varies
s ame
of
understand
to produce
host
resistance
a single
set
environment.
of
obscure.
genetics
diseases
the
of
to
compared to p l a n t s ,
very
to
needed
has a lso
either
as
a
race-specific
and
al.,
K h u s h , I 97 I ;
1 977 ;
Pa n d a
a l . , I 9 83) .
both
pathogens
and h o s t s
23
have g r e a t
v a r i a b i l i t y , and
depends
not
only
pathogen
involving
environmental
on
the
the
genotypes
polygenic
condition's
genetics
in
of
systems,
which
of
resistance
the
but
these
host
also
and
on
the
genotypes
are
g r o w n ( R u s s e l l , I 9 7 8 ).
Ma ny
differ
cases
from
maternal
to
have
one
parents
cytoplasmic
resistance,
example
been found where
other
in
s o me
containing
the
Texas
heavily
in fected
detect
resistance
in
a
to
change
pathogen.
by
wa s
of
case
blight
the
in
All
in
the
is
corn
U. S. A.
c r o s s e s might
due
disease
a good
hybrids
ge ne we r e
in c ite d
by
(Ullstrup,
be n e c e s s a r y
factors.
(1982)
reported
that
the
bacterial
diseases
into
host
toward
by a f e w
of
disease
disease
I 970
reciprocal
According
conditioned
characteristics
the
factors.
hybrids
respective
c y t o p l a s m i c mal e s t e r i l i t y
cytoplasmic
Vanderplank
In
corn l e a f
B e l mi n t h o s p o r i u m m a v d i s
to
their
phenotypic
cytoplasmic
I 97 2 ) . T h e r e f o r e ,
resemble
inheritance.
southern
for
and
reciprocal
more
to
frequent
Brinkerhoff
genes
often
unstable.
In
the
cotton
varieties
with
in
single
to
the
the
in
of
results
the
resistance
bacterial
States,
B genes
b a c k g r o u n d wa s m a t c h e d i n a s e a s o n
plants
virulence;in
(1970),
cotton
United
introduction
blight
re si stance
a susceptible
by i n c r e a s e d v i r u l e n c e
24
in
X a n t h o mg n a s
Vanderplank
succeeded
o a mn e s t r i s
( 1 9 8 2 ),
in
to
m a l v a o e a r u m.
cotton
synthesizing
now a p p e a r s
pv.
breeders
a high
level
Accordi ng
seem
of
to
to
have
resistance
that
be s t a b l e .
Control
According
transluoens
for
could
Jones
be
et
aI .
eliminated
by
t wo h o u r s w i t h f o r m a l d e h y d e
reported
mercury
mercury
the
disease.
The p a t h o g e n i s
compounds
organic
that
therefore
the
has
disease
mercury
considerations.
subtilin
the
disease.
53°
C for
Kg s e e d ) ,
gr/100
diluted
Ki m
hydroxide,
treatment
(Di ckson,
seed)
has
Go o d ma n
KoleVa.(1981)
q'uinolate
treatments.
seed
been
1:1000
30 m i n . ) , 0 . 1
Kg
ounce
c o mp o u n d s
JL*.
ILi.
barley
pv .
seeds
s o l u t i o n . Nuncie (1938)
at
controlling
safety
treating
Ceresan
c o mpounds ;
1/2
(1917)?
that
controlled
of
to
per
bushel
very
treatment
oi
seed,
sensitive
with
organic
used
succesfully
1956).
However,
been
and
provided
reported
that
phytobacteriomycin
Kg s e e d )
hot
to
found
control
water
of
(at
( 2 l i t e r / I 00
( 200
gr/100
were
found
to
tnat
the
bactericide,
registered
and
r e c o mme n d e d
be
us e
due
(1947)
adequate
in
the
prohibited
Henry
to
a nd V i u a v a x
effective
( 200
seed
.
(1982)
had
reported
been
without
evidence
of c o m p l e t e
control.
cupric
for
seed
Accordi ng
25
to
Ma t h r e
(1982),
copper
hydroxide
could
reduce
seed-born
inoculum.
The
use
conditions,
weeds
of
pathogen f r e e
crop
rotation,
susceptible
infested
plant
measures
(Jones
to
debris
et
the
are
al.,
seed
the
produced
destruction
pathogen,
r e c omme nde d
1917;
Boosalis,
and
as
under
of
dryland
perennial
destroying
the
best
control
1952;
and
Ma t h r e ,
1982).
are
Mathre
(1982) r e p o r t e d
that
known,
although
are
others.
s o me
no r e s i s t a n t
more
cultivars
susceptible
than
26
CHAPTER 3
MATERIALS AHD METHODS
Materials
Twenty-three
in
the
crossing
CM 6 7 ,
resistance
In
( Ki m,
this
(I)
to
3) •
Of
191
as.
these
parents
cultivars
( SW 191)
and t he
are
very
r e m a i n d e r h a v e s o me
different
Mo n t a n a
with
and
groups
barley
isolate,
set,
( 2) other
diallel
six
design
cultivate.
wer e H e r t a ,
(Table
2).
used
(3)
or
crosses
X-67, i n
additional
the
resistant
resistant
x
x
crosses.
mating
these
one
crosses,
Crosses
in
three
a complete
resistant
Suweon
wer e
1982).
study,
susceptible
diallel
and
(Table
to the d i s e a s e ,
t e s t e d with
field:
cultivars
program
Kangbori,
susceptible
wer e
barley
Summi t ,
The
bacterial
fully
four
to
the
selected
parents
Betzes,
and
disease
for
used in
cultivars
streak,
the
ma d e
in
investigate
Oderbrucker,
susceptible
as
to
were
Th e p a r e n t s
first
leaf
parents
(Kim,
actions
diallel
set
CM 67 a n d SW I 91
s o me
last
1982).
diallel
gene
the
have
the
a complete
set
t wo
The
resistance
are
very
cultivars
were
chosen
27
Table
2.
Barley c u l t i v a r s
program
Cultivars
Herta
S ummi t
Oderbrucker
Betzes
CM 6 7 ( • )
Suwe on 191 ( • )
Kangbori ( • )
Alpine
Luther
Susceptible
because
of
they
resistant
Al l
since
possible
inheritance
detail.
parents
in
the
Origin
Cl
MT
Cl
Cl
Cl
Swe de n
Engl and
Ge r ma ny
Poland
USA
S . Ko r e a
n
USA
8097
729
4666
6398
1 37 82
Cl 957 8
12 5 5 8
12 5 6 9
1 2577
12595
1 2776
I 2777
12787
1 2866
1 3095
3 8251 I
382650
382720
382732
383077
crossing
Ethiopia
Vl
n
n
Swe de n
n
Ethiopia
fi
n
n
n
n
it
n
varieties
have
Oderbrucker.
as
Numbe r
Cl
Cl
Cl
Cl
Cl
Cl
Cl
Cl
Cl
PI
PI
PI
PI
PI
(*):
used
good a g r o n o m i c
Oderbrucker
1917
(Jones
has
et
been
al.,
crosses
a mo n g t h e s e
of
disease
the
types with
1917;
cultivars
resistance
the
exception
reported
to
and
1 9 82) .
K i m,
were
was
ma de
studied
be
and
in
28
Table
3.
C r o s s e s ma d e
p a r e n t s , F 1s
Cr oss
Herta
n
n
for
and
t h e d i a l l e l s e t and t h e i r
F2 s w h i c h w e r e e v a l u a t e d
Parents
Fis
+
+
+
+
+
+
x
x
x
x
Summi t
Oderbrucker
Betzes
it
CM 67
it
x
SW I 9 1
S ummi t x H e r t a
it
x Oderbrucker
it
x Betzes
it
x CM 67
it
x
SW I 9 1
Oderbrucker x Herta
it
x Summi t
it
x Betzes
it
x CM 67
it
x
SW I 9 1
Betzes x Herta
It
x Su mmi t
it
x Oderbrucker
it
x CM 67
it
x
SW I 9 1
CM 67 x H e r t a
it
x Summi t
it
x Oderbrucker
ft
x Betzes
it
x
SW I 9 1
SW 1 9 1 x H e r t a
it
x Su mmi t
it
x Oderbrucke r
it
x Betzes
it
x CM 67
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
F2 S
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
SW 1 9 1 : S uweon I 9 1
+ : E v al uated
- : Not e v a l u a t e d
In
between
the
second
other
group,
promising
eighteen
resistant
crosses
cultivars
were
ma d e
and one o f
29
the
susceptible
resistant
disease
cultivars
(Table
In
the
different
detect
heritable
whether
resistance
the
to
the
4).
third
if
group,
were
they
had
resistant
crossed
different
cultivars
with
each
genes
wer e grown i n the g r e e n h o u s e
i g 83-84
they
to
for
from
other
to
resistance
H).
,F^s
of
had
origins
determine
(Table
varieties
and
were
checked
true
F^s
during the winter
p h e n o t y p i c a l Iy
or
selfed^
to
Selfed
determine
plants
if
were
eliminated.
Parents,
F^s
Horticulture
serpentine
were
row
( 20
planting
seeds/row).
For
CM 6 7 w a s
spreader
to
were
d e s i g n was
15 cm a p a r t
planted.
of
Fg s
Fa r m n e a r Bo z e ma n ,
were spaced
apart
and
i n rows
T we n t y
each
enhance
used.
at
Individual
3 m i n length
of
each
seeds
the
infection
a n d 30 cm
and F1
planted.
t wo
rows
(Figure
A
plant's
parent
were
between every
uniform
planted
Mo n t a n a on 21 May 1984.
seeds
F g » 120
planted
space
One
as t he
I).
Inoculation
Artificial
(X-67) " o f
inoculation
JL- ILl p v .
barley.
This
barley
field
isolate
at
wa s c a r r i e d
I r 3. n s l u £ £ n a . ,
was
Sidney,
out
highly
obtained
from
Montana,
where
with
a strain
virulent
an
to
irrigated
the
natural
30
Table
H.
C r o s s e s ma de i n t h e r e s i s t a n t x s u s c e p t i b l e and
resistant x resistant categories
and t h e i r
we
r
e
e
v
a
l
u
ated
F2
S
w
h
i
c
h
p a r e n t s , F 1 S 1 a nd
Parents
Cr os s
x Herta (•)
Oderbrucker
Kangbor i
x H e r t a (*)
"
X S ummi t ( * )
"
X Oderbrucker
"
X Kangbor i
I 2 5 5 8 x CM67
I 256 9 x K a n g b o r i
"
12577 x
"
12595 X
"
12776 X
"
I 2777 X
ff
x CM 67
1 27 87 x SW 191
12866 x CM 67
fl
x Kangbor i
13095 x SW 191
"
382511 x
382650 X "
3 8 2 720 x K a n g b o r i
3 8 2 7 3 2 x SW I 91
"
383077 x
Al pi ne
"
"
Luther
Cl
Cl
Cl
Cl
Cl
Cl
Cl
Cl
Cl
PI
PI
PI
PI
PI
X
X
(•)
+: e v a l u a t e d
- : not e v a l uated
(•): resistant x resistant
infection
rate
F2
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
-
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
(*)
F1
crosses
of b a c t e r i a l
leaf
streak is
usually
very
high .
The
bacterium
incubation
wa s
chamber
cultured
at
28°
on W i l b r i n k ' s
C for
3
days
agar
and
in
an
then
(N
O1 CL,
X X
'—I
S
P 1 P2
\
\
I
I
—
\
I
I
\
\
\
\
I
I
I
I
r-
Cl, [l,
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
F 2 (P1XP 2)
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
F 2 (P2X P i)
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
.
.
,
X
X
X
X
X
X
X
X
X
X
X
x
X
X
X
x
X
X
X
X
X
X
X
x
X
X
X
X
X
X
Planting design for a cross of the dial Iel set
P 1P-
—
I
I
I
I
I
I
I
I
I
I
+
+
+
+
+
+
+
+
+
+
rsi
CL,
X
X
X
X
X
X
X
X
X
X
X
CM
CL,
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
S : Spreader row
P 1 : Parent I row
P y : Parent 2 row
F (P.,XP 7) : Normal F 1 row
F (P ^XP^): Reciprocal F 1 row
F~ (P ,%p;): Normal F 2 row
F^ (P 2 < ) : Reciprocal F 2 row
Planting design for
other crosses
fN
P-i
Figure
I.
Planting
desi gn of
field
t e s t , Horticulture
F a r m , B o z e ma n , 1984
32
transferee!
to l i q u i d
shaken
room
at
inoculation,
with
Wilbrink's
temperature
the
bacterial
double
distilled
Plants
wer e
first
was
entries
sprinkler
one h o u r
in
the
spreader
of
10 cm.
All
the
bacterial
The
second
first
the
one,
second
using
a
two
day
disease
wa s
Before
diluted
wa s
1:3
a hand
suspension
water.
the
keep
up t o
the
ten
All
one
a height
after
the
performed,
by
cutting
up
and. s o a k i n g f o r
conditions
for
sprayer.
One w e e k a l t e r
was
rows
CM 6 7
by s p r a y i n g
days
sprinkler
time
of
pump t a n k
prepared
were
to
plants
plants.
spreader
Plots
evening.
by mo wi n g t o
third
stage.
to i n o c u l a t i o n for
The
performed
the
tillering
inoculated
wounding the
from
development
was
early
prior
then
using
inoculation,
intervals
hours.
the
the
wo u n d e d
were
suspension,
at
condition.
wer e
inoculation
in
in
irrigated
entries
leaves
hours
three
r ows ,
bacterial
infected
out
a h u mi d
without
36
suspension
inoculated
carried
to o bta in
for
Th e c u l t u r e
water.
Inoculation
wer e
medi um.
irrigated
favorable
disease
at
for
scoring.
Disease Scoring
The
disease
r ows we r e
an, e ar ly ,
parent,
highly
reactions
infected.
susceptible
were
chosen to
wer e
rated
Fourteen
parent
and
determine
wh e n
the
spreader
Fg p o p u l a t i o n s
a
the
late,
having
resistant
relation
between
33
earliness
and s u s c e p t i b i l i t y .
plants
heading at
ma r k e d
and t h e i r
Th e
( Ki m,
the
1982),
wa s
s a me t i m e
disease
following
In t h e s e
used
as the e a r l y
reaction
index,
to
populations,
the
p a r e n t s we r e
recorded.
partly
based
classify
the
on K i m ’ s s c a l e
plants
for
disease
reaction:
I : No d i s t i n g u i s h a b l e
flag
2:
Short
3;
Me d i u m l o n g
s ympt oms , on b o t t o m l e a v e s .
streak
s ympt oms
on a l l
leaves
except
leaves.
H;
of
streak
s ympt oms .
area
streak
s y mp t o m
on f l a g
leaves,
but
less
than
10
infected.
5:
10 p e r c e n t
of
flag
leaves infected.
6:
30 p e r c e n t
of
flag
leaves in fected .
Y;
50 p e r c e n t
of
flag
leaves infected.
8:
70 p e r c e n t
of
flag
leaves in fected .
9:
90 p e r c e n t
of, f l a g
The
most
individual
highly
p l a n t wa s
leaves infected.
infected
rated
for
flag
leaf
of
every
disease.
Statistical Procedures
Th e f o l l o w i n g
evaluate
I.
were
statistical
procedures
were
used to
data:
Parent
considered
as
and
F^ v a r i a t i o n s
environmental
for
variations.
disease
Ea c h
reaction
plant
34
in
the
parental
deviations
resistant
were
and
deviations
F2
to
rows
assumed
classes.
detect
was
calculated.
susceptible
were
susceptible
used
and
the
Th e
read
In
parent
as t he
the
of
+ twice
r a n g e s of
the
standard
resistant
range
having
standard
ranges
me a n s
reaction
individuals
and
and
of
the
F^
genotype
in
the
degrees
of
the
was
populations.
2.
For
the
do mi nancewere
3.
observed
4.
crosses
calculated
Chi-square
classes
fit
tests
common p a r e n t .
in
had
(Li,
I 955).
were
F ^s ,
used
to
a hypothetical
Ho m o g e n e i t y
segregations
which
te sts
F2 p o p u l a t i o n s
genetic
were
of
determine
done
the
if
the
ratio.
to
crosses
compare
with
one
35
CHAPTER 9
RESDLTS
DAallel
and
The
complete
F2 s
was
Resistant
studied
x
susceptible
dialiel
set
in
with
three
resistant
crosses,
Set
six parents,
different
crosses,
and
( 3)
(2)
their
F^s
groups:
(I)
susceptible
resistant
x
x
susceptible
crosses.
Resistant
Disease
Summi t ,
F2 s
to
Oderbrucker
are
parents
reaction
shown
have
wa s
in
Table
5
were
resistance
Their
and t h a t
and
the
6.
F1s
their
parents
of
The
s a me
found to have
as
Crosses
resistant
a nd B e t z e s )
X- 6 7•
reciprocals,
of
of f o u r
statistically
is o la te
level
x Resistant
their
four
level
and
resistance
including
statistically
parents;
thus
F 1s and
resistant
or
F 2 S,
( H e r t a,
tne
s a me
no s e g r e g a t i o n
detected.
Susceptible
Both
susceptible
statistically
bacterial
leaf
had
tne
streak
x Suceptible
parents
s ame
level
(Table
5).
Crosses
(CM
of
67
and
SW
191)
susceptiblity
Their
F1s
and
to
F2 S ,
36
Table
5.
Disease
reactions
of
parents
Cultivar
disease
reaction.
Cultivar
Herta
S ummi t
Oderbrucker
2 . 7 + I .4
2 . 9 ± 1. 3
2 . 9 ± 1. 3
Betzes
CM 67
SW I 91
including
reciprocals
different
from
apparently
did
their
not
(Herta,
Summit,
susceptible
t wo
groups
67 c ro s s e s
Figure
CM 67
ones
s ta tistic a lly
not
F2
The
+ 1.2
± I .4
± 1.6
populations
( T a b l e 6 ).
between
Crosses
four
Oderbrucker
-
resistant
and
parents
B e t z e s)
and
two
(CM 67 a n d SW 191). w e r e c a t e g o r i z e d i n
according
to
their
susceptible
a n d ( 2 ) SW 191 c r o s s e s
parents:
( T a b l e 7 , 8 , 9,
(I)
CM
a n d 10;
II).
x CM 67
Th e
disease
an i n t e r m e d i a t e
domi nance
significant
and
wa s
susceptibility
F2 s .
set.
Crosses
Herta
of
diallel
diseaes
reaction
were
s Susceptible
crosses,
the
3.0
7.6
7.7
parents.
segregate
Hesitant
These
also
in
reaction
susceptible
calculated
is
of
probably
reciprocal
The F2 p o p u l a t i o n s
as
this
cross f e l l
between
reaction,
and
0 . 1IT • T h i s
indicated
incompletely
differences
segregated
wer e
the
degree
dominant.
found
continously,
in
F^ s
that
No
and
appearing
37
Cr oss
±
I .2
2.3
±
I . 2
±
I .5
2.3
±
I .3
2. 1
I
I .4
2 . I
+
I .4
2 . I
±
I .4
2.5
±
I .5
2.6
±
I .5
±
I . 4
2.9
I
0.7
±
I .0
2.9
2.9
±
0.6
2.7
±
I .0
7-7
+
I .0
7 .7
I
I .2
7-7
2.7
+
I .2
2.9
+
I .3
2.0
+
I . 2
I .8
+
I .3
2.0
±
I .6
±
I .4
2.0
+
I . 4
2.5
+
I .3
3.0
+
1 .0
2.9
+
3. 1
+
I .0
3 • I
7.7
+
I .2
7-7
to
the
+
I .0
+
I .3
+
I .3
+
I .5
2.3
+
I .4
I .0
3.0
+
I .0
±
I . I
3 • I
±
I . I
+
I .3
7.7
+
I .2
I .9
crosses
to
the
c a n be c o n c l u d e d
resistance
0.7
CVJ
it
s kewed
±
CO
slightly
CO
x susceptible
±
co
3-3
O
I .2
in
I
CVJ
polygenic
3-3
CVJ
result,
I .2
CVJ
Fr om t h i s
curves
+
CVJ
nor mal
3.4
O
Susceptible
Bo t h
on
(*):
Reciprocal
on
Hertax
S ummi t
Hertax
Oderbrucker
Hertax
Betzes
S ummi t x
Oderbrucker
S ummi t x
Betzes
Oderbrucker x
Betzes
CM 67 x
SW 191 ( * )
Hertax
S ummi t
Hertax
Oderbrucker
Hertax
Betzes
S ummi t x
Oderbrucker
S ummi t x
Betzes
Oderbrucker x
Betzes
CM 67 x
SW 191 ( • )
Fg
has
No r ma l
the
CVJ
FI
as
D i s e a s e r e a c t i o n s o f F 1 s a n d FpS f o r
r e s i s t a n t x r e s i s t a n t and s u s c e p t i b l e x
s u s c e p t i b l e crosses in the d i a l l e l s et .
rv
Ge n.
6
-Er
Table
susceptible
that
disease.
Hert a
side.
probably
38
Suem it
s
CH 67
No s i g n i f i c a n t
Fgs .
The
F\|
dominance
s h o we d
for
indicates
difference
a susceptible
reaction.
this
that
dominance.
reciprocal
cross
Since
tne
F^
parent
differentiate
individuals
genotype
this
from
reason,
considered
classes,
as
estimated
susceptibility, is
susceptible
Fi
was
value
class,
those
in
of
very
it
tne
individuals
one
group
and
as
another
as
was
was
not
the
tne
a
probablity
Su mmi t
may
have
of
wnich
compl et e
partly
in
tne
possible
to
having the
parent.
6-8
classes
individuals
parent
in
For
were
the
class,
2-4
were
group.
S e g r e g a t i o n i n t h e Fg p o p u l a t i o n f i t
with
to
susceptible
in
degree
0.84
close
which were in the r e s i s t a n t
considered
The
Fg p o p u l a t i o n
the
the
was f o u n d i n
of
one
0.20-0.25.
recessive
This
gene
for
a ratio
or 1:3
indicated
resistance
that
to the
disease.
Oderbrucker
In
the
s CM 67
F^s
differences
and
were
found.
susceptible
reaction
calculated
as
almost
ratio
0.84.
completely
of
1:3 ,
FgS,
and
tne
Thus,
dominant.
1 :6:9
and
7:9
no
significant
F^s
of
degree
this
of
the
susceptibility
reciprocal
cross
domi nance
is
Segregation in the
with
th§
had
a
wa s
probably
F2 f i t t n e
c
i
p r o b a b i l i t i e s of
Table
7.
Cross
Disease re a ctio n s
d ia lle l set.
Parents
disease
of
Disease
parents,
reactions
F 1S and
of
F |S
Herta
x
2
x
CM 6 7
x CM 6 7
CM 6 7
to
3b
2.7*1.3
2 10 4
Oderbrucker
Betzes
I
2 . 8 - 0 .9*
CM 67
Summi t
P
x
2 . 8 *0 .8
2 to
3
3.3*0.9
3 to
P l : Parent I
^2 : P a r e n t 2
N: N o r m a l c r o s s
4
Cm 67
Frequencies
reac t ions
P
Fps for
1
2
of
3
crosses
F 2 s 0:1 d i s e a s e
4
5
N
R
C
5.9*o.9
5.7* I .0
5 . 9 * I .0
N:
0
2
I
5 1 06
5 10 7
R:
0
I
3
C:
0
3
4
9
18
6
in
class
7
the
bases
3
9C
2
7.5-1.I
7 to
8
8 . 0 * I .3
7 to
9
7.9*1.6
7 to
9
7 . 8 * 1 .6
7 to
9
5 to
7
16
40
30
6
2
0
13
14
25
9
9
0
29
54
55
IS
II
0
12
2I
27
10
0
7 . 3- I . 9
0
0
to
0
0
I
9
6
30
38
12
0
0
0
10
27
18
5I
65
22
0
0
0
3
14
6
26
26
2I
0
6
8
7.1*1.6
6
to
8
7 . 5 * 1 .6
7 to
8
7.2*1.5
6
to
8
7.3*0.9
7 to
8
R: R e c i p r o c a l c r o s s
C: C o m b i n e d v a l u e
a: E stim ated v a r i a t i o n
b: A c t u a l v a r i a t i o n
c : D isease c l a s s (I
0
0
7
18
I5
23
16
5
0
0
0
10
32
2 I
49
42
26
0
0
0
5
8
19
36
30
25
0
0
0
0
2
7
13
IS
24
0
0
0
5
10
26
49
48
49
0
to
9)
UJ
VD
Table
8.
P r o b a b l e F 1 g e n o t y p e s a nd h y p o t h e t i c a l
CM 67 c r o s s e s i n t h e d i a l l e l s e t .
Cross
segregations
Probable F 1
Combined classes to detect
genotype
hypothetical segregation
i n F^s of
Ratio
Probability
-
in F 2
Herta x
—
Continous segregation
-
Aa
(1+ 2+ 3 + 4+ 5) : (6 + 7+ 8 + 9)
1:3
0.20-0.25
Aa
(1+2 + 3 + 4 ) : (5 + 6 + 7+ 8 + 9)
1:3
0.25-0.50
1:6:9
0.05-0.10
CM 67
Summit x
CM 67
Oderbrucker
x CM 67
Betzes x
CM 67
AaBb
(1+2+3):(4+5):(6+7+S+9)
AaBb
(1+2+3+4+5) : (6+7+S+9)
AaBb
(1+2+3 + 4 ) : (5+6) : (7 + 8+ 9)
7:9
1:6:9
0.01-0.025
0.90-0.95
I
41
0.25-0.50;
0.05-0.10
Indicate
that
recessive
genes
and
0.01-0.025.
Oderbrucker
for
ma y
have
These
either
results
one
or
t wo
and
tne
resistance.
B e t s e s s CM 67
Th e
degree
whi ch
Fi
of
was
in
dominance
indicates
dominant.
high
that
SB. 1 Ql
susceptible
for
this
has
fit
found
almost
ratio
This
genes
for
for
this
of
as
0. 87»
completely
1:6:9 wi t h
shows t h a t
a
Beuzes
resistance.
Crosses
Herta
s SH 191
No F 1 p l a n t w a s t e s t e d
that
the
class
represents
This
the
of
Th e
F2 which
F1 c l a s s ,
suggests
dominant.
that
has
the
did
continously.
Herta
resistance
to
leaf
corresponds
to
. SUDBit
bacterial
result
of
the
not
frequency
domi nance
is
is
0. 59«
incompletely
fit
any
ratio
probably
has
polygenic
streak.
This
cross
of H e r t a
and
conclusion
x CM 67«
z SH I 91
No s i g n i f i c a n t
F 1 S and
whi ch
of
I f we a s s u m e
highest
susceptibility
F2 p o p u l a t i o n
the
cross.
the
degree
segregated
the
was
is
the
( P= 0 . 9 0 - 0 . 9 5 ) .
t wo r e c e s s i v e
category,
cross
susceptibility
The F2 p o p u l a t i o n
probability
probably
the
s h o ws
F 2 S.
that
reciprocal
The d e g r e e
of
differences
wer e
d o m i n a n c e wa s
susceptibility
is
found
in
c o mp u t e d a s 0. 48
incomletely
domi nant .
I
Table 9. Disease reactions of parents,
diallel set.
Cross
Parents disease
reactions
P1
Herta x
SW 191
Summit x
SW 191
Oderbrucker
x SW 191
2.8-0.8
2 to 3
-
-
-
7 to 8
3.2-0.8 8.0-1.4
3 to 4
Frequencies of F- on disease class bases
I
2
3
4
S
6
7
8
9C
Disease reactions of F.s
R
C
N
p2
2.0-1.637. 6-1. Ob
I to 3
F 1s and F 2S for SW I 9 1 crosses in the
7 to 9
7.3-1.4
6 to 8
N:
0
4
3
7
19
27
20
13
0
R:
0
2
6
10
11
35
27
11
0
C:
0
6
9
17
30
62
47
24
0
6.2-1.4
6.7-1.0
6.4-1.3
0
0
3
10
4
28
25
19
0
5 to 7
6 to 7
5 to 7
0
0
10
7
12
33
13
6
2
0
0
13
17
16
61
38
25
2
0
6.2-1.I
S to 7
6.4-1.8
6.2-1.2
0
I
15
14
10
11
18
7
5 to 7
5 to 7
0
3
14
16
11
14
19
4
0
0
4
29
30
21
25
37
11
0
Betzes x
3.1-1.6
7.7-1.6
7.0-1.I
7.5-1.4
7.1-1.I
0
2
3
5
8
7
25
6
0
SW 191
2 to 3
7 to 9
6 to 8
7 to 8
6 to 8
0
4
5
7
11
9
33
9
0
0
6
8
12
19
16
58
15
0
R: Reciprocal cross
b: Actual variation
Pg: Parent 2
Cr Combined value
c: Disease classes ( I to 9)
N: Normal cross
a: Estimated variation
: Parent I
-Fn
IX)
Table
10.
P r o b a b l e F 1 g e n o t y p e s and h y p o t h e t i c a l
SW 1 9 1 c r o s s e s i n t h e d i a l l e l s e t .
Cross
segregations
Probable F 1
Combined classes to detect
genotype
hypothetical segregation
Ratio
in F? s of
Probab.
in F 2
Herta x
SW 191
Summit x
Continous segregation
_
Aa
(1 + 2 + 3 + 4) : 15+6 + 7+ 8 + 9)
1:3
0.05-0.10
Aa
(1+2+3):(4+S+6+7+8+9)
1:3
0.25-0.50
AaBb
11+2+3+4):15+6+7+8+9)
7:9
0.25-0.50
AaBb
(1+2 + 3) : (4 + 5+ 6) : (7 + 8+ 9)
1:6:9
0.10-0.20
-
SW 191
Oderbrucker
x SW 191
Betzes x
SW 191
Probab.: Probability
The F2 p o p u l a t i o n
of
0.05-0.10.
has
one
fit
Thi s
recessive
the
ratio
result
gene
of
I :3 w i t h
indicates
for
that
a probability
S u mmi t
r e s i s t a n c e , whi ch
t h a t of t h e c r o s s of Summi t
probably
agrees
with
a n d Fg r e s u l t i n g
from
x CM 6 7 .
O d e r b r u c k e r x SH 191
Th e
disease
reciprocal
those
of
crosses
normal
reaction,
0.75,
were
F^
might
indicate
probability
t wo
fit
significantly
a n d F 2 . The
degree
F2 p o p u l a t i o n
of
not
and t h e
whi ch
one or
reactions
the
of
showed
dominance
almost
Thus,
resistance
from
a susceptible
wa s e s t i m a t e d
compl et e
r a t i o s , of 7:9
( P= 0 . 2 5 - 0 . 5 0 ) .
recessive
F^
different
and
domi nance.
1: 3 w i t h
Oderbrucker
as
The
the
s a me
ma y
have
genes.
B e t z e s x SH 191
In
the
F^s
and
Fg s ,
d i f f e r e n c e s were found.
in
the
wa s
susceptible
calculated
completely
1:6:9
with
h a s , two
as
dominant.
the
class.
The
Susceptiblity
genes
of
degree
is
0.10-0.20.
for
reciprocal
cross
was a l m o s t
of
domi na nc e
probably
Th e Fg p o p u l a t i o n f i t
probability
recessive
significant
The F 1 o f t h i s
parent
0. 86.
no
the
Betzeg
resistance.
almost
ratio
of
probably
The
c o n c l u s i o n w a s m a d e f o r t h e c r o s s o f B e t z e s x CM 6 7 -
same
Herta x CM 67
H e r ta x
SW 191
Summit x CM 67
Summit x
SW 191
Oderbrucker
x CM 67
Od erbrucker
x SW 191
Betzes x CM 67
Betzes x
SW 191
F i g u r e I I . F^ d i s t r i b u t i o n s o f CM 67 and SW 191 c r o s s e s i n t h e d i a l l e l s e t . P ^ :R e s i s t a n t
p a r e n t ' s c l a s s . P2 : S u s c e p t i b l e p a r e n t ' s c l a s s . F^:F^ c l a s s . I t o 9 :D is ea s e
c l a s s e s i n F2 *
H eaA stant z S u s c e p t i b l e
In
this
resistant
three
The
and
category,
to
bacterial
susceptible
results
18.
are
to
promising
leaf
cultivars
shown
These
according
s o me
their
streak
(CM 6 7 ,
Table
crosses
C rosses
11,
barley
were
cultivars
crossed
with
SW I 91 a n d K a n g b o r i ).
12,
13,
were
studied
susceptible
parents.
I 2) ,
in
15,
16,
three
17
groups
CM 67 Crosses
Three
different
crosses
according
to
homogeneity
segregated
differently
w e r e ma d e w i t h
test,
(Table
their
F2
11 a n d 1 2 ;
CM 6 7 ,
and
populations
Figure
III).
Cl 1 2 5 5 8 z CM 67
The
is
degree
close
to
may
leaf
have
domi nance
zero,
intermediate.
segregated
of
and
wa s
indicates
The F2 p o p u l a t i o n
continously.
polygenic
estimated
The
did
result
intermediate
that
not
as
0. 13
whi c h
resistance
fit
any
s h o we d
that
resistance
to
ratio
Cl
is
and
12558
bacterial
streak.
Cl 1 2 7 7 7 Z CM 67
Th e
Fi
of
reaction.
Th e
indicates
that
this
cross
degree
of
showed
dominance
susceptibility
F2 p o p u l a t i o n
fit
the
probabilities
of 0 . 2 5- 0. 50
almost
ratios
is
was
partially
of 7:9
and
a susceptible
0.70,
which
dominant.
1:6:9
and 0 . 0 5 - 0 . 1 0 . Thus,
with
The
the
Cl 1 2 7 7 7
Table
11.
Disease r e a c t i o n s of p a r e n t s ,
r e s ista n t x susceptible cross
Cross
Pa re nts d i s e a s e
disease
CM 67
Cl 12777
I t o 3b
X
CM 67
Cl 12866
CM 67
X
‘
O
I . 9-0 .9
2
3
4
4.5-1.7
0
3
11
22
14
12
7
7
0
0
I
10
9
17
12
15
12
I
20
16
17
9
10
12
I
I . 5-1 .0
8 . 0- 1.3
6 .5-1.4
I to 2
7 to 9
6 to 7
I to 2
a: Estima ted v a r i a t i o n
b: Actual v a r i a t i o n
Frequencies o f F^ on d i s e a s e c l a s s bases
1
3 to 6
I . 5-1 .0
CM 67 c r o s s e s
reaction
7 to 8
O
X
I +
Cl 12558
in
I +
t—
reactions
F 1s and F2 S f o r
category.
-
7 to 8
c : D is eas e c l a s s e s
0
5
6
7
8
9C
0
in
the
Table
12.
Probable
g e n o t y p e s a nd h y p o t h e t i c a l s e g r e g a t i o n s i n F 2 S o f
CM 67 c r o s s e s i n t h e r e s i s t a n t x s u s c e p t i b l e c a t e g o r y .
Cross
Probable
Combined classes to detect
genotype
hypothetical segregation
Ratio
Probability
in F 2
Cl 12558
X
-
Continous segregation
-
AaBb
il+2+3+4+5):16+7+8+9)
7:9
0.25-0.50
AaBb
(1+2):(3+4+5):(6+7+S+9)
1:6:9
0.05-0.10
-
CM 6 7
Cl 12777
X
CM 67
Cl 12866
CM 67
X
Aa
(1+2+3+4+5):(6+7+S+9)
3 :1
0.50-0.75
AaBb
(1+2+3+4):(S+6+7+8+9)
9:7
0.25-0.50
may h a v e
t wo r e c e s s i v e
genes f o r
resistance.
£ 1 1 2 B66 £ £M S i
In
this
cross,
populations
fit
probabilities
the
of
Cl 12866
Six
the
ratios
that
resistant
Cl
test
same ma n n e r
3:1
resistance
C rosses
lines
were
(Table
13,
and
is
9:7
The
and
PI
14 and
the
segregation
domi nant
with
Sw
Fg p o p u l a t i o n s
3 83077
15;
Fg
resistance.
crossed
the
The
with
partially
t wo g e n e s f o r
SH 191
3 82732
tested.
0.25-0.50.
s h o we d t h a t
1 3 0 9 5 , PI
was
of
a nd
may h a v e o ne o r
The h o m o g e n e i t y
I 27 87 ,
plant
0.50-0.75
o f t h e Fg i n d i c a t e s
and
no
191.
o f Cl
segregated
Figure
in
III).
Cl 1 2 7 8 7 & S I 191
Th e
parent
0.61.
Fi
of
class.
This
this
The
degree
shows t n a t
The Fg p o p u l a t i o n
the
fit
probabilities
may h a v e o ne o r
£ 1 13095
No
s
of
reacted
of
near
dominance
tne
was
resistant
computed
resistance
is
partially
the
of
3 : 1 and
ratios
0 . 5 0 - 0 .7 5 a n d
t wo d o m i n a n t
resistant
dominant.
12:3:1
0.25-0.50 .
as
Cl
with
1 27 87
genes.
M R 191
Fi
plant
segregation
dominant.
cross
in
Wi t h
was
the
Fg
tested
for
suggests
that
t h e s ame p r o b a b i l i t y
Fg p o p u l a t i o n f i t
the r a t i o s
this
cross.
resistance
( P= 0 . 5 0 - 0 . 7 5 ) ,
o f 3:1. a n d 1 2 : 3 : 1 -
Th e
is
the
Cl 1 30 95
Table
13.
Ho mo g e n e i t y t e s t
cross category.
Cross
for
SW I 91 c r o s s e s
Phenotypes of F 2
in
D .F .
the
resistant
Chisquare
x susceptible
Probability
(12:3:1 expected)
R
I
S
Cl 12787 x
0: 75.00
18.00
10.00
SW 191
E : 77.25
19.31
6.44
Cl 13095 x
87.00
22.00
5.00
SW 191
85.50
21.38
7.12
81.00
15.00
5.00
75.75
18.94
6.31
55.00
15.00
10.00
60.00
15.00
5.00
PI 382732 x
SW 191
PI 383077 x
SW 191
Total
Summed data
298.00
7 0.00 30.00
298.50
74.63 24.87
Homogeneity
2
2.12
0.25-0.50
2
0.68
0.50-0.75
2
1.46
0.25-0.50
2
5.42
0.05-0.10
8
9.68
2
1.35
0.20-0.25
6
8.33
0.20-0.25
R rResistant
S :Susceptible
I :Intermediate
D .F . :Degrees of freedom
O :Observed
E :Expected
Table
14.
Cross
D i s e a s e r e a c t i o n o f p a r e n t s , F 1s a nd F 2 S f o r
the r e s i s t a n t x s u s c e p t i b l e c r os s c at e gor y.
Parents d isease
reactions
?
Cl 12787 x
SW 191
Cl 13095 x
F
disease
I
reaction
3
4
5
6
7
8
9
19
27
14
15
8
10
5
5
0
-
0
58
29
5
7
10
4
I
0
12
26
19
10
I
2
3
3
0
2
20
13
12
7
13
7
7
0
-
28 . 19
22
12
8
7
4
I
0
-
14
17
11
7
8
8
2
0
(f
1 . 4 - 1 . I 3 8 . 6- 1.5
I t o 2b
7 to 9
3.4-1.I
3 to 4
2 to 3
7 to 9
PI 382511 x I . 5 - 1 . I
6 .9-1.5
3.6-1.0
I to 2
6 to 8
3 to 4
PI 382650 x I . 5 - 1 . 0
6.9-1.7
3 . 0 - 1 .6
I to 2
6 to 8
2 to 4
PI 382732 x I . 3 - 1 .0
7.8-1.3
SW 191
SW 191
I to 2
7 to 9
PI 383077 x I . 2-0 .9
7.7-1.5
SW 191
I to 2
a : Es ti m a te d v a r i a t i o n
b: A c t u a l v a r i a t i o n
7 to 9
c: D is e a s e c l a s s e s
13
in
on d i s e a s e c l a s s base s
2
7. 5 - 1 . 4
SW 191
Z
I
2 . 1- 0 .7
SW 191
Fre que nc ie s of F
SW 1 9 1 c r o s s e s
Table
15.
Probable F1 genotypes
SW 1 9 1 c r o s s e s i n t h e
Cross
Cl 12787 x
SW 191
Cl 13095 x
SW 191
PI 382511 X
SW 191 X
PI 382650 X
SW 191
PI 382732 X
SW 191 X
PI 383077 X
SW 191 X
Probablle F
genotype
a nd h y p o t h e t i c a l s e g r e g a t i o n s i n F ^ s o f
r e s i s t a n t x su sceptible category.
Combined classes to detect
hypothetical segregation
in F 2
Ratio
Probability
Aa
AaBb
Aa
AaBb
AaBb
AaBb
AaBb
(1+2 + 3 + 4) : 15+ 6+ 7+6 + 9)
U+2 + 3 + 4) : (5+ 6) : (7 + 8+9)
v1+ 2+ 3) : (4 + S+ 6+ 7 + 8+ 9)
U+2+3) : (4 + 5+ 6) : (7 + 8+ 9)
(1+2) : (3 + 4+ 5) : (6+ 7 + S + 9)
(1+ 2+ 3 + 4+ 5 ) : (6+ 7 + S+ 9)
(1+2+3+4): t5+6+7+8+9)
3:1
12:3:1
3 :I
12:3:1
9:6:1
15:1
9:7
0.50-0.75
0.25-0.50
0.50-0.75
0.50-0.75
0.20-0.25
0 . 10- 0.20
0.50-0.75
AaBb
Aa
Aa
AaBb
(1+2+3+4):(5+6):(7+8+9)
11+2+3+4):(5+6+7+S+9)
(1+2+3+4) : t5+6+7+8+9)
(1+2+3+4):(5+6):(7+8+9)
12:3:1
3 :I
3 :1
12:3:1
0.25-0.50
0.20-0.25
0 . 10- 0 .2 0
0.05-0.10
53
Cl 12558 x CM 67
Cl 12787 x SW 191
Cl 12777 x CM 67
Cl 13095 x
Cl 12866 x CM 67
PI 382511 x
SW 191
PI 582650 x SW 191
PI 382732 x
SW 191
SW 191
PI 383077 x
SW 191
Fi gur e I I I . F7 d i s t r i b u t i o n s of CM 67 and SW 191 c r o s s e s i n t he
r e s i s t a n t x s u s c e p t i b l e c a t e gor y. P ^ i Re s i s t a n t p a r e n t ' s
c l a s s . P2 : Su s c e p t i b l e p a r e n t ' s c l a s s . F
^
class.
54
ma y h a v e
either
modifying
genes
of. t h e
e
.
reaction.
shows
genes
this
that
or
dominant
gene
resistant
being e p i s t a t i c
cross
with
resistance
and
0.10-0.20.
dominant
s ome
genes with
to the
one
other „
showed a m o d e r a t e l y
might
interm ediate.
9:6:1
dominant
t wo
resistant
resistant
The d e g r e e o f d o m i n a n c e w a s e s t i m a t e d
dominant
and
dominant
SE 1S.L
The F I o f
ratios
or
dominant
UL 382511
which
one
15: 1
PI
genes
with
The
the
3 8251 1
for
Fg
ma y
with
incompletely
population
probabilities
have
resistance.
genes i n t e r a c t
be e i t h e r
two
fit
of
the
0.20-0.25
incompletely
In the f i r s t
each
as 0.39
case,
both
other.
P I 3 8 2 6 5 0 a SE. I S l
Th e
disease
resistant
reaction
parent
calculated
class.
The
as 0.61,
which
partially
dominant.
With
0.75),
Fg p o p u l a t i o n
the
may h a v e
t wo i n c o m p l e t e l y
of
the
F^
degree
indicates
a high
fit
was
of
close
to
the
dominance
was
that
resistance
probability
the
ratio
dominant
or 9:7-
genes f o r
( P=
is
0.50-
PI 382650
resistance.
2 1 3 8 2 7 1 2 z SE IQI
Parents
and
Fg w e r e
tested
for
this
'
population
fit
the
ratios
probabilities
of
show t h a t
barley
this
0.25-0.50
of
and
12:3:1
and
0.20-0.25.
l i n e ma y h a v e o n e o r
cross.
The Fg
f.
3: 1
Th e
two
with
the
results
dominant
55
genes f o r
is
resistance.
incompletely
If
PI 3 8 2 7 3 2 h a s
one g e n e ,
the
gene
tested.
With
the
the
F2
dominant.
PX 383077 i SB 121
For
this
cross,
the
F2
fit
the
0 .10-0.20
ratios
segregation,
dominant
genes.
dominance
modifying
is
If
PI
it
of
has
resistant
cultivar
varieties
Figure
IV).
12777
with
or
segregated
might
there
According
have
may
one
or
to
two
dominant
gene,
be
other
some
Crosses
Kangbori
and s e v e n
Kangbori
test
in
fit
indicated
the
same
wa s
crossed
lines
(Table
of A lp in e ,
with
17 a n d
Luther,
18,
a n d Cl
the
same
that
t h e F2 of t h e s e
crosses
(Table
and
manner
ratio
t wo
16,
(9:6:1).
17
A
18;
IV).
A lpine s
Kangbori
The r e a c t i o n
class.
of
the
The d e g r e e
indicates
dominant.
the
12:3:1.
resistant
The Fg p o p u l a t i o n s
homogeneity
which
and
genes.
Susceptible
parent
3: 1
one
incomplete
was
and
383077
Kangbori
Figure
plant
O
population
of
FI
O
I
in
O
O
probabilities
no
that
F^ w a s f o u n d
of
resistance
The F 2 p o p u l a t i o n
probability
of
dominance
0.20-0.25.
fit
This
is
the
in the
wa s
resistant
estimated
almost
ratio
indicates
as
completely
of 9:6:1
that
with
Alpine
0.82,
Table
16.
Homogeneity
category.
Cross
test
Kangbori
Phenotypes of
(9:6: I
Alpine x K
for
O:
E:
Luther x K
Cl 12777 x K
Total
Summed data
2
F2
expected)
R
I
50.00
45.00
46.00
52.88
40.00
47.25
23.00
30.00
41.00
32.25
37.00
31.50
7.00
5.00
7.00
5.88
7.00
5.25
136.13 101.00
145.13 96.75
21 00
16.13
Cl 12777 x K
Cl 12866 x K
Total
Summed data
Homogeneity X 2
107.00
99.00
D .F .
in the
resistant
Chisquare
x susceptible
ProbabiIity
S
Homogeneity X
(9:7 expected)
54.00
4 7.25
53.00
51.75
crosses
30.00
36.75
39.00
40.25
69.00
77.00
2
2.99
0.20-0.25
2
2.05
0.25-0.50
2
2.66
0.25-0.50
6
2
7.70
2.23
0.25-0.50
.
4
5.47
0.20-0.25
I
2.18
0.10-0.20
I
0.07
0.75-0.90
2
I
2.25
1.46
I
0.79
0.25-0.50
57
may h a v e
t wo
dominant
genes f o r
resistance.
Laatfaieir % Kangfoori
The
The
F1 showed a r e s i s t a n t
degree
suggests
of
that
dominance
resistance
probability
of
9:6:1
Therefore,
ratio.
dominant
genes
was
is
Alpine,
tne
as
disease.
0.99.
dominant.
segregation
like
to
computed
comietely
0.25-0.50,
for
reaction
of
the
Luther
This
Wi t h
Fg
may
the
fit
have
a
t wo
resistance.
JGZ ] 2 5 6 9 z Kangfoori
Dominance
indicates
that
Fg p o p u l a t i o n
0.05-0.10.
and
its
deviation
was
resistance
is
fit
a 1:2:1
Probably,
effect
is
Cl
calculated
probably
ratio
wnich
intermediate.
with
the
one
gene
1 2 569 h a s
as 0.25,
The
probability
for
of
resistance
intermediate.
£ 1 1 25 7 7 z Ka n g f o o r i
The F 1 r e a c t i o n
between
degree
that
not
the
of
susceptible
dominance
resistance
fit
an 1 : 2 : 1
0.025-0.05
Further
parent.
to
which
study
is
is
bacterial
and r e s i s t a n t
was
estim ated
interm ediate.
ratio.
is
to
than
s t r e a k was found'
parent
as
0.13
classes.
which
The
shows
The Fg p o p u l a t i o n
The p r o b a b i l i t y
lower
needed
leaf
did
was c o m p u t e d as
an
acceptable
determine
inheritance
level.
in
this
Table
I?
Disease r e a c t i o n s of p a r e n t s ,
re sista n t x susceptible cross
Cross
Alpine x
Kangbori
Parents disease
!•'
d i s e a s e
1
2
3
I .9-I.3a 7.9-1.3
2.8-1.3
9
20
21
8
8
7
7
0
0
0
3
43
16
16
9
7
0
0
0
10
23
10
4
10
10
3
0
2
21
22
12
15
7
4
0
0
-
5
9
26
24
12
13
2
2
0
0
8
25
17
9
13
13
4
0
4
13
23
14. 10
13
7
0
0
4
18
17
14
11
17
10
I
0
18
25
18
15
6
8
6
0
0
I to 3b
2 to 3
7.7-1.3
2.8-0.4
Kangbori
2 to 3
7 to 9
2 to 3
Cl 12569 x
I.2-0.9
7.4-1.3
3.9-1.6
Kangbori
I to 2
6 to 8
3 to 5
Cl 12577 x
I.5-1.4
6.8-1.I
4.3-1.4
Kangbori
I to 3
6 to 8
3 to 5
Cl 12595 x
2.0-1.I
7.7-1.0
Kangbori
I to 3
7 to 8
Cl 12776 x
2.4-1.I
7.8-0.8
6.2-I. 5
Kangbori
2 to 3
7 to 8
5 to 7
Cl 12777 x
I.7-1.0
7.6-1.0
2.5-1.I
7 to 8
5 to 7
I to 2
Cl 12866 x
I.5-1.0
7.5-1.0
Kangbori
I to 2
7 to 8
PI 382720 x- I.4-1.3
Kangbori
7.3-1.6
a: Estimated variation
b: Actual variation
-
3.8-1.7
c : Disease classes
4
in
the
on disease class bases
reaction
7 yo 9
Kangbori
Frequencies of
crosses
reactions
2.8-0.5
Luther x
F 1 s a nd FpS f o r K a n g b o r i
category.
5
6
7
8
9C
CJl
CO
Table
18.
Probable
Kangbori
Cross
Probable F I Combined classes to detect
genotype
hypothetical segregation
in F 2
Ratio
Probability
U+2+3) : (4 + 5+6) : (7+ 8+ 9)
9:6:1
0.20-0.25
(1+2+3):(4+5+6):(7+8+9)
9:6:1
0.25-0.50
(1+2):(3+4+5):(6+7+S+9)
1:2:1
0.05 -0.10
(1+2):(3+4+5):(6+7+S+9)
1:2:1
0.025-0.05
(1+ 2+ 3+ 4) : (5+ 6) : (7 + 8+ 9)
(1+ 2+ 3 + 4 ) : (5+6 + 7+ S + 9)
12:3:1
3 :I
0.10-0.25
0.10-0.20
AaBb
AaBb
Aa
(1+ 2+ 3) : (4 + 5+ 6) : (7 + 8+ 9)
(1+2+3):(4+5+6+7+S+9)
(1+2+3+4):(5+6+7+S+9)
9:6:1
9:7
3:1
0.25-0.50
0.10-0.20
0.25-0.50
AaBb
(1+ 2+ 3 + 4 ) : (5 + 6+ 7+ S+ 9)
9 :7
0.75-0.90
Alpine x
AaBb
Kangbori
Luther x
AaBb
Kangbori
Cl 12569 x
A 1A 2
Kangbory
Cl 12577 x
A 1A 2
Kangbori
Cl 12595 x
AaBb
Kangbori
Aa
Cl 12776 x Unknown
Kangbori
Cl 12777 x
Kangbori
PI 382720 x
Kangbori
Cl 12866 x
Kangbori
F 1 g e n o t y p e s a nd h y p o t h e t i c a l s e g r e g a t i o n s i n F 2 S o f
crosses
in the r e s i s t a n t x s u s c e p t i b l e c a t e g o r y .
60
CX 1 2 5 9 5 2L K a n g b o r i
No
p l a n t was t e s t e d f o r t h i s
probabilities
ratios
Cl
of
3 •*1 a n d
12595
genes
ma y
for
The
12:3:1.
have
calculated
as
incomletely
0. 54
dominant.
susceptible
in
the
F2 p o p u l a t i o n
did
Cl 12 7 7 7 s
Kangbori
degree
ratios
not
F I of
fit
indicate
incompletely
completely
9=6:1
0. 50
and
two
dominant
and
0.10-0.20.
the
that
dominant
found
of
that
any
most
showed
was
dominant.
of
d o m i n a n c e wa s
wa s
the
is
closer
individuals
reaction.
a resistant
computed
to
the
as
bacterial
The
indicates
for
to
The
F2
ratio.
resistance
This
closer
susceptibility
a resistant
9=7 w i t h
genes
was
The d e g r e e
class,
s howed
cross
that
cross
indicates
dominance
suggest
of
results
A l t h o u g h t h e F^ r e a c t i o n
fit
this
of
class.
parent
population
almost
two
this
which
the
is
or
of
parent
to
results
The a b o v e
one
reaction
susceptible
The
F2 p o p u l a t i o n
Kangbori
Fi
The
the
sim ilar
resistance.
Cl 1 2776 2
the
( P= 0 . 1 0 - 0 . 2 0 ) ,
c r o s s . With
reaction.
0.84.
These
leaf
streak
F2 p o p u l a t i o n
fit
the
probabilities
or 0.2 5-
that
may
resistance
Cl
to
I 2777
the
have
disease.
Cl 1 28 66 z. K a n g b o r i
Parents
and
F2 w e r e
tested
for
this
cross.
Wi u h
a
61
Luther x
Alpine x
Cl 12569 x
Kangbori
Kangbori
Cl 12577 x Kangbori
Cl 12777 x Kangbori
Kangbori
Cl 12595 x
Kangbori
Cl 12776 x
Kangbori
Cl 12866 x
Kangbori
PI 382720 x
Kangbori
Figure IV. redistribution of Kangbori crosses in the resistant x
susceptible category. P^:Resistant parent's class. P2:
Susceptible parent's class. F ^ F 1 class.
62
high
probability
a 9:7
ratio.
might
have
recessive
( P= 0 , 7 5 - 0 . 9 0 ) ,
This
t wo
leads
to
dominant
homozygote
the
genes
masks
the
conclusion
for
the
F2 p o p u l a t i o n
tnat
resistance
erfect
of
the
fit
Cl 1 2 0 6 6
and
either
other
gene.
PX 3 8 2 7 2 0 z KangborJL
The F i r e a c t i o n
that
of
the
to the d i s e a s e
resistant
dominance
was
resistance
is
probably
population
fit
the
0.25-0.50.
one
estimated
The
dominant
parent
with
this
suggest
for
resistant
parents
( Table
parents
had t h e
which
that
degree
indicates
dominant.
the
of
tnat
The
F2
probability
or
PI 3 8 2 7 5 0
may
have
Pealsfcanfc C r o s s e s
Alpine
and
Luther
were
crossed
which
were
used
Oderbrucker,
the
diallel
same l e v e l
set.
Statistically,
of r e s i s t a n c e
to
the
as
all
disease
17).
The
reaction
of
not s i g n i f i c a n t l y
the
and
in
The
resistance.
category,
He r t a , S u m m i t
0,31
of 3 : I w i t h
^esJLafcaiat z
In
class.
incompletely
ratio
results
gene
as
w a s f o u n d t o be n e a r
cultivars.
cultivars
used
or
F^ s
differ
The
in
gene
Another
possibility
from each
results
this
c ommon
a nd F2 S t o
closely
is
linked
the
strain
other
suggest
category
that
the
and f r o m
that
ma y h a v e
genes
size
( X-67) did
for
of
tne
at
that
of
parent
least
one
resistance.
Fg p o p u l a t i o n s
Table 19. Disease reactions of parents, F 1 s and F2 S for
the c r o s s e s in the r e s i s t a n t x r e s i s t a n t
category.
Cross
Fo
F1
Alpine x
Herta
Alpine x
Oderbr.
Luther x
Herta
Luther x
S ummi t
Lu th er x
Oderbr.
I -7
I
I -9
I
1 .9
I
I .6
I
I .5
I
±
to
±
to
±
to
±
to
±
to
2.8
2
2.4
I
2.0
I
2.3
I
2.0
I
I .0
2
I .4
3
I .4
3
I .I
2
I .0
2
+
to
±
to
±
to
±
to
+
to
2 -8 ±
2 to
I -7 ±
I to
2 -3 ±
2 to
-
0.9
3
I .5
3
I .2
3
I .6
3
I .4
3
2 -3 ±
I tO
I -7 ±
I to
I .4 ±
I to
2 .0 +
I to
I -7 +
I to
I .0
3
I .0
2
I .0
3
I .4
3
I .5
3
I -3
3
1.8
4
I .5
3
Oderbr.: Oderbrucker
as
not
large
enough
to
detect
segregations.
Relation between Earlineas and Susceptibility
The
in
disease
reactions
I iJ F 2 p o p u l a t i o n s w h i c h
and
an e a r l y , s u s c e p t i b l e
each
disease
class
populations,
early
higher
the
in
the
with
resistant
plants
Cl
Cl
12 5 9 5 ,
plants
had a l a t e ,
computed
(Table
percentages
classes
Thus,
susceptibility.
were
recorded
resistant
Their
plant
classes.
early
parent.
susceptible
resistant
associated
were
of
percentages
in
20).
all
F2
to
be
zero
in
were
earliness
In
found
and l o w e r
However,
parent
or
was
s ome
mostly
early
and
w e r e o b s e r v e d i n t h e F 2 p o p u l a t i o n s ot
I 27 87 ,
PI 38251 I , a n d
PI 3 83077 -
Table
20.
D i s e a s e c l a s s f r e q u e n c i e s a n d p e r c e n t a g e s o f e a r l y p l a n t s i n 14 F 2
p o p u l a t i o n s which have a l a t e ,
r e s i s t a n t p a r e n t and an e a r l y ,
susceptible parent.
C r o s s e s
I
B
A
D.C.
D
E
28(0)
14(0)
C
19(0)
2
27(7)
58(7)
19(5)
13(23)
3
16(6)
14(14)
29(0)
22(5)
17(24)
11(55)
4
5
6
7
8
9
17(35)
7(71)
8(75)
9(44)
10(90)
5(20)
15(33)
10»70)
10(90)
12(83)
1(100)
-
12(0)
I
J
K
L
M
N
2(0)
9(0)
5(0)
4 (0)
18(0)
11(0)
26.12)
20(5)
3 (0)
21(0)
10(0)
9(0)
16(0)
25(0)
21(1)
19(16)
13(6)
21(5)
10(40)
12(50)
-
2(0)
-
43 (0)
22(9)
23(0)
26(19)
17 (0)
18(11) 21(8)
8(25)
16(13)
12(25)
10(20)
24 (36)
14(14)
15(33)
13(29)
8(63)
16(44)
15(73)
4 (0)
12(51)
11(0)
9(59)
6(71)
8 i38)
7(71)
1(100)
7(29)
6(63)
2(100) 13(46)
7(57)
9(78)
7(71)
10(70)
13(75)
17(76)
6(86)
8(43)
3(100)
7(86)
7(100)
7(57)
4(50)
10(70)
2(50)
10(70)
6(83)
3(100)
7(100)
3(67)
2(50)
5(60)
4(75)
4(50)
8(63)
5(40)
1(100)
1(100)
2(100)
7(100)
-
-
-
1(100)
-
-
'
D.C. :Discase classes
E
:PI
383077
xSW191
J :C1 12577 x Kangbori
A :CI 126G6 x CM 67 c
F
:PI
382511
x
K :CI 12569 x
X :Mean
a !Actual frequencies
B :CI 12767
G
:PI
382650
x
L :CI 12595 x
b !Early plant percentages in each class
H
:Alpine x Kangboric
M :CI 12866
c :Early, susceptible parents
X
SW 191°
C :CI 13095 x
D :PI 382732 x
“
I iLuther x
X
20 (0)
12(0)
a b
20(0)
H
G
k'
X
hi !PI 382/20 x
9(66)
3(66)
65
CHAPTEB 5
DISCUSSION
Disease
As
Boosalis
disseminate
of
Developnent aad
( I 95 2)
bacterial
a diseased
water-congested.
cultivar
(CM
experimental
high
adequate
inoculum
growing
season.
of
reason
was
Early
of
one
one
one
planted
the
is
wnen
very
rows
Hall
et
aI .
X a n t - h o m -Oja-ae £ a . f f l x e s i n i s
pv.
i n a n a l i l i i e ns was
within
days.
39
observed
that
inoculated
supported
two
rows
irrigation
(i)
Bockelman
the
row
the
to
meters
disease
to
the
promoted
By s p l a s h i n g
the
from
uniformly
provided
through
the
tnat
capable
infection
spread
row.
only
His
of
louus
cells
from
tne
observation
row b e t w e e n e v e r y
infection.
infection
bacterial
caused
p e r s o n a l . communication)
of a s p r e a d e r
the
two
reported
a single
(1984,
uniform
rows
(1981)
adjacent
planting
create
adjacent
are
every
and
the
28 s q u a r e
both
inoculation
spreader
to
susceptible
for
spreading
ways
by c o n t a c t
between
artificial
these
of
barley
a healthy
this
row
rows.
infection
streak
with
For
6.7)
reported,
leaf
plant
P l a a t i n a Design
process
from
Sprinkler
in
two
ways:
infected
plant
66
rows to the o th e rs ,a n d
(ii)
surface
bacterial
Th e
thus
factors
infection
enabling
mentioned
by c r e a t i n g de w On t h e
above
and e l e m i n a t e d
helped
small
blocks
blocks
reduces
Thus,
and
parents,
small
area
provided
which
uniform
belonged
different
due
I).
to
a
uniform
individuals
c ro s s were
A serpentine
the
stratification
environmental
environment
to
create
field
of
a n d Fg o f o n e
(Figure
a
that
evaluation
error
and i n v a s i o n .
escapes.
G a r d n e r (1961) s u g g e s t e d
in
movement
plant
influence.
planted
planting
by l o c a l i z i n g
same
cross
within
yet
in a
design
individuals
were
in
the
blocks.
E a r l i r a e a s and S u s c e i o t i b l i t v
Early
classes
that
plant
were
had
there
(the
frequency
might
to
the
in
showed
the
early
and
the
I 4 Fg
parent
that
one
or
susceptible
Fg
population
be a g e n e t i c l i n k a g e
susceptibility.
susceptible
susceptible
This
in
in
be h i g h e r
early,
parent.
phenotypes
higher
found
an
resistant
percentages
However,
there
populations
and
tne
one)
a
was
earliness
other
late
parental
indicating
between
are
disease
in
a
that
and
possible
explanations:
1)
humidity
In e a r l y
are
adequate
summer,
for
because
bacterial
temperature
infection,
and r e l a t i v e
disease
67
development
is
conditions
worsen
down
or
stop
plants
ma y
escape
from
true
the
sprinkler
until
Levitt
early
photosynthetic
plant
for
rates,
is
provide
plant.
to
3)
conditions,
X,
o.
navy
pv.
opportunity
carried
favorable
out
for
be
every
disease
that
high
growth
rate
of
high
rate.
The m e t h o d
available
to
an
early
The y
its
high
et
stomata
al.
et
s ome
al.
disease
for
reach
supported
ha d b e e n
of
always
reached
time,
growth
This
enter
the
which
will
the
above
resistance
related
to
stomata.
found
we a s s u m e
of
to
pathogens
populations
a function
bacteria
in
(1980)
ana
longer.
instances
symptoms
If
open
(19. 8 0)
reviewed
to
photosynthetic
o p e n i n g and c l o s i n g
to
was
may n o t
a
Dhaseoli
are
speculation
might
to
bean l e a f l e t .
bacteria
ones
season.
reported
opportunities
Weller
and l a t e
early
related
and s u s c e p t i b i l i t y
of
result,
d ire c tly
keep
more
the
a
may s l o w
is
Campbell
time
in
m aintaining
conclusion.
the
The a b o v e
perhaps
and t h a t
As
infected
irrigation
late
plants
bacterium
conditions
(1980)
progresses,
development.
highly
keep
season
the
disease.
to
development
2)
for
become
days
As t h e
disease
because
three
rapid.
that
that
were
under
detected
field
alter
5 x I 0& c e l l s
population
bacteria
will
a su ffic ie n t quantity
sizes
per
of
h a v e mo r e
on l e a v e s o f
68
early
heading
earlier
All
in
If-
plants,
a nd
longer.
or
some o f
a close
is
and
linkage,
their
PI
exposed
barley
s ome
cultivars
may
be
early
to
infection
a b o v e may h a v e r e s u l t e d
a nd
linkage
Cl
susceptibility.
betw een
1 25 95,
promising
resistant
Cl
for
these
1 27 87 ». PI
breaking
plants
were
this
found
in
crosses.
In h eritan ce of
The
crosses
set
are
factors
genetic
383077
since
they
between e a r l i n e s s
a
characteristics,
382511,
the
relation
there
since
results
with
the
suggest
Oderbrucker,
action
obtained
four
that
gene
crosses
of H e r t a w i t h
Vanderplank
segregation
characteristic
these
effect
having
of
numbers
the
chromosomes,
(I)
could
three
the
the
the
in
in
SW 191
the
dialiel
H erta,
same w i t h
(Table
and
Fg
may be d i f f e r e n t
7 » 8,
9 ana
populations.
five
Resistance
reasons
may
be d e t e r m i n e d
times,
third
gene;
(3)
characteristic
be
for
in
continous
to
continous
polygenic;
other
in
1 0 ) . . The
According
by t h r e e
and t h e
Summ it,
r e g a r d to gene
CM 67 a n d SW I 91 s h o w e d
(1982),
are:
is
CM 67
parents
r e c e s s i v e ) , but
to
.in
the
re sista n c e
regard
segregation
from
resistant
and B e t z e s
(resistance
R esistan ce
genes,
two
three
(2)
the
one o f
times,
the
different
may be d e t e r m i n e d
oy a
69
block
and
of
three,
the
gene
presence
and two l i n k e d
effects
of
a
resistance
are
large
can
without
take
explained
discount
4th
The S u m m i t
Summit
ma y
bacterial
67 a n d
one
two
the
ratios
one
have
the
been
gave
the
(Table
the
ratio
recessive
Th e
that
was
mentioned
population.
performed
this
for
reason
found
As
in
a
we may
from
Oderbrucker
their
the
resistance.
fit
be
the
F2
and
x SW 1 91 f i t
c ommon i n
CM 67
This
and
populations
th a t Betzes
to
I '3
susceptible
Fg
CM
either
The
both
different.
with
to
witn
may h a v e
1:3 was
to
crosses
suggests
resistance
Oderbrucker
different
with
for
CM 67
of
resistance
results
of
Although
Betzes
This
gene
x
that
were
by
genes f o r
Although
underlie
factors
Oderbrucker
genes
8),
results
1:6:9.
monogenic
can
s a me
For
The c r o s s e s
10).
caused
s a me
the
( 4)
CM 67 a n d SW 191 s h o w e d t n a t
Oderbrucker
latter
backgrounds.
all
in
recessive
streak.
1:3 a n d 7 : 9 ( T a b l e
crosses,
or
environment.
crosses with
of
additive;
effect;
experiment
recessive
segregation
some
gene,
assumption.
have
leaf
and
dominance
together
SW 1 91 i n d i c a t e d
or
1:6:9;
(5)
place
uniform
the
same,
complete
before,
relatively
the
environmental
c o n t i no u s v a r i a t i o n ;
above
g e n e s and a s i m p l e
both
may
genetic
SW I 9 1
fitting
ma y h a v e t w o
disease.
resistant
x susceptible
70
crosses
in
the
resistance
among
these
segregate
the
gene
to
in
their
In
in
that
the
9:7
especially
of
crosses
significantly
that
common r e s i s t a n c e
genes
is
on
the
that
to
true
s ame
the
F2
detect
for
the
the
do
not
gave
7:9
parents
two
(Table
contain
segregation
in
As
the
caused
either
by
results
s howed
that
any
the
gave
all
Herta
the
of
and
that
polygenes
12777
or
or
sim ilar
results
and
SW 1 9 1 ) .
genes.
cross
The Fg p o p u l a t i o n
of
Cl
Cl 1 2 7 7 7
12866
before,
Fg p o p u l a t i o n
also
crosses
x susceptible
that
of
The
these
(CM 6 7
results.
explained
Cl
same
Bo t h o f
resistant
set
and SW 191
resistance
continously,
1:6:9,
12).
CM 67
susceptibles
a variety
and
cross in the d i a l l e l
Fg p o p u l a t i o n s .
Cl 1 2 5 5 8 s e g r e g a t e d
ratios
one
enough
addition,
CM 6 7 c r o s s e s i n
category
not
the
T h i s may i n d i c a t e
least
large
is
resistant
segregations
probably
did
possibility
x susceptible
segregate.
four
suggest
parents,
resistant
not
This
inheritance
s i n c e H e r t a may h a v e p o l y g e n i c r e s i s t a n c e .
susceptible
with
linked
were
segregations.
not
parents
Another
populations
did
in four
p a r e n t s have a t
chromosome.
showed
Fg p o p u l a t i o n s .
different
crosses,
set
be d i f f e r e n t
resistant
resistant
or
d iallel
of
Cl
other
probably
the
fit
fit
the
3:1
and
continuous
12558
might
factors.
has
or
two
be
These
recessive
71
genes,
a n d Cl 1 2 8 6 6 ma y h a v e e i t h e r
genes
for
resistance
separate
resistance
to
genes
12777,
in
Cl
or l o o s e l y
may be u s e f u l
bacterial
linked
parents
one o r
for
leaf
a n d Cl
loci
two d o m i n a n t
streak.
12866
, then,
combining
are
If
the
located
these
at
cultivars
the genes.
Th e c r o s s e s o f SW I 9 1 i n t h e r e s i s t a n t x s u s c e p t i b l e
category
g a v e some s i m i l a r
and some
Th e F 2 p o p u l a t i o n s o f Cl 1 2 7 8 7 ,
PI
383077
crosses,
fit
the
s a me
a homogeneity
t o be h o m o g e n e o u s .
could
the
they
ratios
have
same
either
effect
have
the
same
program
type
other
and
populations
ratios.
from
the
one
shows
each
that
PI
other
and
the
resistance
linked
or
at
program
Kangbori
category
the
genes
same
to
segregated
locus,
combine
crosses
of
in
the
the
either
these
lines
is
assumed
that
to the
disease,
in a
it
the
best
be
382650
382511
from
found
with
should
PI
were
genes
If
genes
and
these
different
which has
382511
that
and
For
and t h e y
or
results.
PI 3 8 2 7 3 2 ,
12:3:1).
suggest
resistance.
resistant
PI
and
done
s a me g e n e s
Unless
breeding
wa s
characteristics
of
This
different
the
Cl 1 3 0 9 5 ,
(3:1
The r e s u l t s
for
breeding
test
different
the
used.
fit
and
PI
these
lines
they
can
resistant
sim ilarly
different
four
are
be
are
lines.
closely
used
in
a
genes.
x
or
The F 2
382650
first
resistance
agronomic
susceptible
differently.
72
Alpine,
9:6:1.
they
is
Luther,
Th e
a mutant
1 2 777
the
of
latter
to
a similar
12866
were
12).
This
different
in
gene
the
disease
genes
then,
the
in
the
those
various
In
in
12777
to
located
and
x Kangbori
and
leaf
was
streak.
found
to
be d i f f e r e n t
in
is
assumed
that
the
separate
have
and Luther, c r o s s e s .
to
Cl 1 2 8 6 6 ,
or
loosly
Cl
(Table
12866
other
at
of
x CM 67 c r o s s
Cl
in
found to
those
each
it
t h e F2
segregated
from
If
ratio,
showed t h a t
and
s ame
CI
a 9:7
1 2 866
cross
c r o s s e s were found
crosses
or
bacterial
12866
Alpine
the
Cl 12777 w e r e
Cl
tn at
The F g
crosses
128 6 6
of
Since Luther
to have
Cl
test
Cl
Cl
of
Alpine or L u th er,
12595 and,
of
ratio
suggested
a 9:6:1
that
resistance
the
streak.
Cl 1 2 8 6 6
that
for
resistance.
are
likely
leaf
effects
in
indicates
Kangbori
above
as
test
Cl 1 2 7 7 7 x CM 6 7 c r o s s
dominant
than
are
either
s a me
fit
resistance.
the homogeneity
The F2 s e g r e g a t i o n
other
fit
Cl 1 2 777 a n d
genes
different
they
bacterial
the
manner,
recessive
genes f o r
cross
being
crosses
a homogeneity
s a me
genes
of
12777
Alpine,
Although
population
Cl
of
the
x Kangbori
cross.
be
result
may h a v e
resistance
and
be
The
from
regard
to
resistance
linked
loci,
Cl 1 2 56 9 , Cl 1 2 5 7 7 ,
Cl
PI 3 8 2 7 2 0 s e e m t h e b e s t p a r e n t s t o c o m b i n e t h e
resistance
conclusion,
genes
there
to
bacterial
are
diverse
leaf
streak.
resistance
sources
73
for
that
bacterial
some
of
different
needed
leaf
these
genes
to
streak
of
sources
on t h e
s a me
determine
barley.
This
study
showed
may h a v e i d e n t i c a l
genes or
chromosomes.
study
identical
linked
Futher
and
is
independent
genes.
The Osie o f
Barley
cultivars,
Betzes,
Alpine,
12777,
Cl
3 826 50 ,
PI
3 827 20 ,
streak.
Herta
and
remainder
and
To d e v e l o p
used
ones
to
varieties
by
PI
13095,
3 83077,
resistance
appear
the
t o have
with
to
Cl
382511,
PI
found
oligogenic
in
desired
agronomic
leaf
resistance.
time,
the
can s c r e e n e d
for
a p r o b l e m . Th e n ,
resistance
be
resistance,
a snort
resistances
is
to
bacterial
polygenic
cultivars
the
Cl 1 2 5 9 5 ,
PI
were
disease
transfer
the
characters
to
must
should
commercial
backcrossing.
for
no d i f f e r e n t i a l
ma y be p o s s i b l e
polygenic
for
Cl
Oderbrucker,
Cl 1 2 5 6 9 ,
Cl 1 2 5 5 8 may h a v e
Th e f o l l o w i n g
germplasm
and
oligogenic
where
resistant
12866,
Sources
Summit,
Cl 1 2 5 5 8 ,
resistant
with
resistance
be
Cl
sources
cultivars
He r t a ,
Luther,
12787,
promising
the
^esistaaee
procedure
long-lasting
strains
of
to i d e n t i f y
background
by
can
be a p p l i e d
disease
tne
to
resistance.
bacterium
are
major r e s is ta n c e
screening
develop
Although
known,
it
genes in a
plants
in
an
74
environment
severity
such as
is
polygenic
Sidney,
Montana,
where
v e r y h i g h . H e r t a a n d Cl 1 2 5 5 8 ,
resistances,
By b a c k - c r o s s i n g ,
can
major
be
used
genes
in
as
the
may h a v e
recurrent
parents.
cultivars
loci
carried
background
I 2558.
can
be
the
polygenic
in
Herta-background
without
ma de
major
losing
using
Cl
genes
developed
as
later
lines
polygenes.
1255 8.
in
steps
with
by
resistant
and
Cl
sources.
background
c a n be
a n d Cl
of Herta
inter-crossing
type of
Th e n , . r e s i s t a n t
Herta-
of H erta
different
The s a me
identified
for resistan ce
Major genes in the p o ly g e n ic
combined
disease,
that
as p o s s i b l y h a v in g d i f f e r e n t
into
the
lines
the
major
genes
crosses
c a n be
with
I 2558-background
combined
can
be
75
CHAPTKB 6
SOm&BZ
was
Inheritance
of
resistance
investigated
in
23
d i a ll el
set
susceptible
FIs
and
with
and
Fg s
isolate
barley
six
( X-67) of
bacterial
cultivars.
parents
resistant
were
to
x
and
23
with
Xanthomonas
I n one
other
resistant
inoculated
leaf
complete
resistant
crosses,
one
streak
parents,
Montana
camoestris
pv.
x
barley
transluoens
in the f i e l d .
Parents,
F^s
and
FgS
to g e th e r in a sm all
area.
(CM 6 7 )
was p l a n t e d
as the
Before
the
and
wounded.
Inoculation
bacterial
three
only
the
suspension.
da y i n t e r v a l s .
infection
severity
I to 9 s c a le
disease
was
susceptible) .
was
the
used to
reactions
plants
Disease
(I:
cross
in every
entries
in the
spreader
classify
completely
cultivar
third
were
row.
sprinkler
rows were
out
spraying
by
sprinkler
reaction
grown
spreader
carried
were
were
susceptible
spreader
all
Plots
of
each
One v e r y
inoculation,
irrigated;
of
wa s
rows
irrigated
rated
wa s v e r y
plants
in
the
resistant;
wh e n
at
the
high.
case
9:
A
of
very
76
In the
reaction
as
the
o f Fi
ranges
means
+ twice
ranges
was
resistant
to
detect
by c a l c u l a t i n g
and h o mo g e n e i t y
of
adjacent
rows
rows
irrigation
the
and
promoted
bacterial
the
helping
bacterial
mentioned
by
experimental
F 1S and Fg3 of
disease
reaction
Most
of
found
a ttrib u te d
the
to
be
to
characteristics.
population
size
resistant
from
in
the
F1
a
Chi-
determine
gene
high
season.
plant
uniform
the
Sprinkler
rows
to
surface
All
the
thus
factors
infection.
by p l a n t i n g
and
for
by s p l a s h i n g
invasion.
together
infection
inoculum
plant
the
and
of
The
parents,
comparing
their
area.
plants
in
This
linkage
Beside
of
on
in
susceptible.
the
have
values.
process
infected
a small
early
caused
reduced
cross
to
sustained
de w
wa s
which
that
cultivars.
growing
movement
each
used
infection
resulted
classes;
deviation
were
the
the
error
susceptible
The d e g r e e o f d o m i n a n c e w a s
of
creating
above
assumed
were
individuals
provided
cells
and
deviations
inoculation
through
others,
were
and
tests
artificial
sp.reader
parents
dominance
n u m b e r s a n d common g e n e s
Early
and s u s c e p t i b l e
standard
i n Fg p o p u l a t i o n s .
estimated
square
of
used
genotype
of r e s i s t a n t
linkage,
pathogen
the
I it Fg
relation
betw een
stomatal
could
be
populations
was
strongly
these
two
opening
and.
involved.
In
77
order
to
develop
bacterial
leaf
1 27 8 7 ,
3 825 1 1 ,
PI
resistant
The
that
is
screak,
plants
however,
ma y
R esistance
recessive
Betzes.
they
in
different
their
reaction
that
a mo n g
Mor e
one
bacterial
Cl
leaf
by p o l y g e n e s
set
Oderbrucker
regard
to
is
needed
to
numbers.
Herta,
and two r e c e s s i v e
common
and
one o r two
genes in
indicated
resistance
that
gene
or
genes.
12777
and
streak.
in
Cl
parent
12866
Resistance
Cl 1 2 5 5 8 ,
determine
(CM 67)
differ
is
in.
probably
by t w o r e c e s s i v e
Cl 1 2 7 7 7 a n d by t w o d o m i n a n t g e n e s i n
study
suggested
(recessive),
in
cultivars
and
and B e t z e s
gene in Summit,
these
Cl
be u s e d .
gene
a common s u s c e p t i b l e
12558,
early
should
action
to
12595,
gave
polygenic
resistance
Cl
diallel
gene
in
Oderbrucker
least
Cl
conditioned
genes in
to
probably
linked
to
Summit,
different
The c r o s s e s w i t h
showed
f r o m . the
be
at
that
Fg p o p u l a t i o n s ,
regard
crosses
v arieties
cultivars,
3 83077 ,
by o n e r e c e s s i v e
The
have
PI
Herta,
genes in
resistant
Barley
with
is
conditioned
and
obtained
resistance
same
and
in
results
the
early
the
Cl 1 2 8 6 6 .
possibility
of
linkage.
Results
susceptible
1 3 0 95 ,
PI
of
resistant
cultivar,
382732
SW 191,
and
PI
line
crossed
suggest
383077
ma y
that
have
with
Cl 1 27 87,
one
or
the
Cl
two
78
dominant
genes
resistance
conditioning
ma y h a v e
gene
two
indicated
dominant
of
commen
effects.
PI
resistance
Kangbori
crosses
that
effects.
that
Cl 1 2 5 6 9 ,
and one
sources
of
Cl 1 2 8 6 6 ,
or
or
have
different
38251 1 a n d
genes
PI
with
3 826 50
different
for
be t h e
ma y
genes are
susceptible
resistant
cultivars
s a me o r
be
different
Kangbori
determined
there
genes in
are
identical,
streak.
or d i f f e r e n t
study is
linked,
by
two
gene in
PI 3 8 2 7 3 0 .
diverse
leaf
with
crosses
by o n e i n t e r m e d i a t e
bacterial
Futher
the
other
ma y h a v e i d e n t i c a l
t h e s a me c h r o m o s o m e s .
these
that
of
a n d Cl 1 2 7 7 7 ma y h a v e t w o
t wo d o m i n a n c e
s howed
barley
sources
some
from
resistance
genes in
study
might
Progeny
dominant
This
with
(one
A lpine, Luther
genes which
suggested
if
in
interactions.
cultivars)
these
like
dominant
Result
like
genes
needed to
resistance
So me
of
genes in
determine
or in d e p e n d e n t .
79
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