Diclofop-methyl interactions with soil-borne fungal pathogens in wheat
by Mary M Kleis
A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in Plant
Pathology
Montana State University
© Copyright by Mary M Kleis (1984)
Abstract:
Herbicide applications can influence disease development. There is some evidence that applications of
diclofop-methyl to diseased wheat may increase expected levels of crop injury. Using the soil-borne
fungal pathogens Bipolaris sorokiniana, Cephalosporium gramineum,. Fusarium culmorum, and
Gaeumannomvdes graminis, this research evaluated: (1) Changes in virulence and growth alterations in
response to diclofop-methyl, (2) Existence of interactions in wheat under field conditions, (3) Effects
of diclofop on wheat root growth in the presence of G. graminis.
Field evaluations compared wheat response to diclofop-methyl in artificially inoculated plots versus
uninoculated plots. Wheat was treated with 0, 1.12, and 2.24 kg ai/HA diclofop-methyl. Fungitoxicity
tests measured the effect of diclofop-methyl at 0, 1, 10, 100, and 1,000 mg/1 on mycelial growth.
Changes in virulence were evaluated after pathogen exposure to 100 mg/l diclofop-methyl. Interactions
between diclofop-methyl and (G. graminis were evaluated in a hydroponic system, where root length,
dry weight and volume were measured.
Data from field studies showed no increases in expected levels of herbicide or disease injury with
diclofop-methyl applications to infected wheat. Conversely, B. sorokinian-diclofop-methyl interactions
resulted in yield increases. In fungitoxicity tests diclofop-methyl inhibited fungal growth, except in the
case of graminis where growth stimulation was noted at 10 mg/1 diclofop-methyl. However, results
from G. graminis-diclofop-methyl hydroponic studies showed no increased root injury due to
diclofop-methyl application to infected wheat. Further field evaluations of G. graminis-diclofop-methyl
interactions are necessary. No changes in virulence of these pathogens were noted after
diclofop-methyl exposure. D IC LO FOP -M ETH YL
INTE RA CTI ON S WITH
SOIL-BORNE FDNGAL PATHOGENS IN WHEAT
by
MARY M KLEIS
A thesis submitted in partial fulfillment
of the requirements for the degree
of
Master of Science
in
Plant Pathology
MONTANA STATE UNIVERSITY
Bozeman, Montana
June I984
APPROVAL
of a thesis submitted by
MARY M KLEIS
This thesis has been read by each m e m b e r of the
thesis c o m m i t t e e and has been found to be satisfactory
regarding c o n t e n t , English usage, f o r m a t , citations,
bibliographic style, and consistency, and is ready for
submission to the College of Graduate Studies.
Date
Chairperson,
Graduate Committee
Approved for the Major Department
Date
Head, Major Department
Approved for the College of Graduate Studies
Date
Graduate
Dean
J
ill
STATEMENT OF PERMISSION TO USE
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the requirements for a master's degree at Montana State
University,
I
agree
that
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Library
shall
make
available to borrowers under rules of the Library.
it
Brief
quotations from this thesis are allowable without special
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provided
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accurate
acknowledgment
of
source is made.
Permission
for
extensive
quotation
from
or
reproduction of this thesis may be granted by my major
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or
in
his
absence,
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Director
of
Libraries when, in the opinion of either, the proposed
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of
copying
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or
material
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thesis
Any
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financial gain shall not be a l lowed w ithout my written
permission.
iv
' TABLE OF CONTENTS
APPROVAL............................................
ii
STATEMENT OF PERMISSION TO US E ....................... . iii
TABLE OF CONTENTS.....................................
iv
LIST OF TABLES........................................
vi
LIST OF FIGURES.......................
ABSTRACT...............................................
viii
ix
INTRODUCTION................................
I
LITERATURE REVIEW.....................................
6
Herbicide -Pathogen Interactions................
The Herbicide Diclofop-Methyl....................
6
I3
MATERIALS AND METHODS........................
The Pathogens................ '...................
Field Studies With Cephalosporium
gramineum............... ................ . .
Field Studies With Fusarium culmorum
and BiPolaris sorokiniana............... .
Field Studies With Gaeumannomvces
graminis................... ................
Greenhouse Studies With Gaeumannomvces
graminis....................................
Studies on Fungitoxicity of Diclofop...........
Studies on Diclofop Induced Virulence
Changes...................................
RESULTS...... '........................................
Field Studies With Cephalosoorium
gramineum...................................
Field Studies With Fusarium culmorum
and Bioolaris sorokiniana.................
Field Studies With Gaeumannomvces
graminis
17
I7
17
I9
22
23
25
26
29
29
31
36
V
TABLE OF CONTENTS--Continued
Greenhouse Studies With Gaeumannomvoes
graminis................. ■..................
36
Diclofop Fungitoxicity Studies.................
Virulence Tests............
37
I
DISCUSSION.............................................
42
SUMMARY......................................... ......
49
LITERATURE CITED......................................
50
APPENDIX
55
vi
LIST OF TABLES
Page
Table
1
2
3
4
Effect of Oephalosporiuni gramineuro
.on y i e l d of thr e e w i n t e r w h e a t
cultivars at Bozeman and Moccasin,
Montana
in I 9 8 2 ................ .
3O
Effect of Diclofop-methyl on yield
of winter wheat uninoculated or
inoculated with C e p h a l o sporium
........................... -....... .
30
Effect of BiPQlaris sorokiniana or
Fnaarium o u l m o r u m inoculation on
yield of Fortuna spring wheat at
Moccasin and Bozeman, Montana......
31
Effect of Diclofop-methyl on yield
of Fortune spring wheat u n i n o c u ­
lated or inoculated with Fbsarium
cuImorum............................
5
Effects of diclofop-methyl on yield
of
Fortune
spring
wheat
uninoculated or inoculated with
Bi pol a r is s o r o k i n i a n a ,.... '
......
6
Effects of Bioolaris s o r o k i n i ana
inoculation on percent disease,
percent severe disease, and wheat
population at Bozeman and Moccasin,
Montana in 1 982............. .......
7
Effects of Fusarium culmorum inocu­
lation on percent disease, percent
severe disease and wheat population
at Bozeman and Moccasin, Montana in
1 9 8 2 ..................... ..........
32
vii
LIST
OF TABL ES --C on tin ue d
Table
8
9
10
11
Page
Effects of treatment with diclofopmethyl on root v o l u m e , dry weight
and. length of Butte spring w h e a t ,
w i t h or w i t h o u t G a e u m anno m vces
g r a m i n i s i n o c u l a t i o n ......................
37
E f f e c t s of d i c l o f o p - m e t h y l and
diclofop-methyl I formulation blank
on radial growth of Gaeumannomvces
graminis. Cephalosnorium eramineum,.
Fusarium c u l m o r u m . and Binolaris.
. sorokiniana...................................
38
Radial g r o w t h of G a e u m a n n o m v c e s
graminis . Cephalosnorium gramine_u_m.
Fusarium c u l m o r u m an d pipolaris,
sorokiniana on media amended with
formulated d i c l o f op-methyl versus
formulation
additives
without
diclof op-methyl.............................
41
Crowning
season precip ita tio n
during 1 982 and 1 983 at Bozeman and
M o c c a s i n , M o n t a n a ......................
55
viii
LIST OF FIGUR ES
Figure
I
?
Page
C h a n g e s in root v o l u m e and dry
weight in response to d i o l o f opmethyl in healthy versus Gaeumannom v c e s e r a m i n i s i n f e c t e d •B u t t e
spring
w h e a t ...................... ......
39
Changes in adventitious root length
in response to d i c l ofop-methyl in
healthy
versus G a e u m a n n o m v e e s
eraminis infected Butte spring
wheat........................................
40
ix
ABSTRACT
H e r b i c i d e a p p l i c a t i o n s can i n f l u e n c e d i s e a s e
development.
There is some evidence that applications of
diclofop-methyl to diseased wheat may increase expected
levels of crop injury.
Using the soil-borne fungal
pathogens
Binolaris
sorokiniana. Cenhalosporium
g r a m i n e u m . F u s a r i u m c u l m o r u m . and G a e u m a n n o m v d e s
g r a m i n i s . this r e s e a r c h e v a l u a t e d : (I) C h a n g e s in
virulence and growth alterations in response to diclofopmethyl , (2) Existence of interactions in wheat under
field conditions, (3) Effects of diclofop on wheat root
growth in the presence of CL. graminis.
F i e l d e v a l u a t i o n s c o m p a r e d w h e a t r e s p o n s e to
diclofop-methyl in artificially inoculated plots versus
uninoculated plots.
Wheat was treated with 0, 1.12, and
2.24 kg ai/HA diclofop-methyl.
Fungitoxicity tests
measured the effect of diclofop-methyl at 0, I, 10, 100,
and 1,000 mg/1 on mycelial growth.
Changes in virulence
were evaluated after pathogen exposure to 100 mg/1
diclofop-methyl.
Interactions between diclofop-methyl
and (L_ graminis were evaluated in a hydroponic system,
where root length, dry weight and volume were measured.
Data from field studies showed no increases in
expected levels of herbicide or disease injury with
d i c l ofop-methyl applications to infected wheat. C o n ­
versely, IL_ s o r o k i n i a n a -diclofop-methyl interactions
resulted in yield increases. In fungitoxicity tests
d i c l ofop-methyl inhibited fungal growth, except in the
case of ili. graminis where growth stimulation was noted at
10 mg/1 diclofop-methyl.
However, results from IL.
g r a m i n i s - d i c l ofop-methyl hydroponic studies showed no
increased root injury due to diclofop-methyl application
to infected wheat.
Further field evaluations of CL.
graminis-diclofop-methyl interactions are necessary.
No
changes in virulence of these pathogens were noted after
diclofop-methyl exposure.
I
INTRODUCTION
Selective
growth
of
herbicides
plants
processes.
In
are
through
addition
chemicals
disruption
to
effects
which
of
on
alter the
biochemical
higher
plants,
herbicides can affect other organisms including fungi.
The
interrelationship
herbicides
incidence
may
or
influenced
betw e e n
lead
to
severity.
by
the
fungal
changes
Disease
direct
in
pathogens
plant
disease
epidem i o l o g y
effect
of
and
can
be
herbicides
on
individual pathogens, as well as by the indirect activity
of
herbicides
environment
on
the
host
(Katan and Eshel,
pla n t
and
in
the
soil
1973; Altman apd Campbell,
1977) .
In cereal crops less research had been conducted on
pathogen-herbicide interactions than with other higher
value crops.
This is probably due to the fact that in
temperate
zones
relative
to
tomatoes,
potatoes,
action
fewer
other
studies
pesticides
crops
such
etc.
conducted
Most
are applied
as
cotton,
to cereals
peas,
bean,
herbicide-pathogen inter­
in cereals
have
emphasized
the
effect of phenoxy herbicides on cereal diseases.
In Montana,
to
wheat
for
phenoxy herbicides are commonly applied
the
control
of broadleaf
weeds
(N issen,
2
1 9 83)-
In
stantial
addition
acreage
to
broadleaf
is treated
phenoxy
herbicides
weeds.
Diclofop-meth.yl
p h e n o x y )phenoxy)
diclofop,
for
the
with
herbicides,
one of
control
(methyl
propanoate,
of
a
s ub­
several
annual
non-
grassy
2-(4-(2*.4,-dichloro-
hereafter referred
to as
is one of the newest grass herbicides reg i s ­
tered for use in cereals.
Use of diclofop is increasing
in Montana as well as in other wheat producing areas of
the world (E. Faust,
cide
personal communication). This herbi­
selectively controls annual grassy weeds in cereals
including,
wild
oat
(A v e n a
f a t 'ua ),
green
foxtail
(Setaria viridis). yellow foxtail (Setaria lutecens), and
annual ryegrass (Lolium m ultiflorum).
Field observations have indicated that there may be
interactions between diclofop and some common soil-borne
cereal diseases.
An increased incidence of Take-All of
wheat
in d i c l o f op-treated fields has been observed in
Chili
(R. Madariaga,
personal communication).
In Oregon
increased diclofop damage in wheat may have been related
to interactions with unidentified soil-borne pathogens
(P. Olson,
personal communication).
Diclofop can reduce root grow t h in wheat and other
grasses.
Growth
restrictions
adventitious roots (Donald et al.,
have
been
1 982)..
observed
in
Affected roots
3
are
shorter
and thicker
appearance
pruning.
after
of
the roots
than normal roots.
The nubbed
is often
to as root
referred
Since pruned roots do not resume
initial
herbicide
exposure,
normal growth
diclofop
applications
could decrease the absorptive capacity of the plant and
reduce
crop
vigor
(Morrison
et
al.,
1981).
Although
wheat roots can be damaged by diclofop exposure,
reductions are not generally observed.
yield
However,
when
combined with other root growth reducing factors such as
plant
disease,
disease
may
the
additive
significantly
effects
affect
of herbicide
wheat
growth.
and
Diclofop
root pruning when combined with pathogen infection may
account for the increase in crop injury which has been
observed with diclofop applications to diseased wheat
(Madariaga
disease
and Olson).
Yield
losses.due
interactions may be greater than those caused
individually by either diclofop or
Those
diclofop
borne
to herbicide-
plant
pathogens
disease.
likely
to
interact
with
to cause increased crop damage are the soil-
root
infecting
fungi.
In Montana the pathogens
commonly infecting wheat and reducing root growth and/or
water
utilization
Fusarium
include
nulmorum.
Gaeumannomvces
eraminis
Ce Dha l o s norium
Bioolaris
var.
tritici
gramineum f
s o r o k i n i a n.a .
a nd
(Dubbs ,and Mathre,
I 979) .
Cephalosporium
winter wheat.
gramineum
is a vascular pathogen of
Infection results in a physical reduction
in internal water m o v e m e n t , and causes localized water
shortages
within
the plant (Morton and M a t h r e , I 980).
Infected plants are stunted with chlorotic leaves,
eventually
produce
ghriveled
kernels.
Both
and
Binolaris
sorokiniana and Fusarium culmorum can infect whgat roots,
causing the disease known as dryland (common) root rot.
These organisms cause root, crown, and subcrown internode
necrosis
leading
to
a reduction
in plant
vigor.
The
effects of infection are thought to be severe under dry
conditions when the diseased roots are unable to obtain
sufficent water to sustain plant growth.
Severe subcrown
internode necrosis can disrupt water m o v e m e n t from the
seminal
roots
to
the
leaves,
causing
internal
water
deficits which may be an important yield reducing factor
under
hot
disease,
dry
conditions
(Wiese,
I 977).
Take-All
caused by Gaeumannomvces graminis var. tritici.
can be severe under irrigation or in high rainfall areas.
The fungus causes necrosis of the roots and crown, there­
by inhibiting water and nutrient transport (Wiese, 1977).
Since
the
relationships
between
soil-borne
gens and diclofop are poorly understood,
patho­
the intent of
5
this research was to investigate these possible interac­
tions.
The
fungi
evaluated
w e r e : IL, s o r o k i n i a n a . F .
c u l m o r u m . C. e r a m i n e u m and G. s r a m i n i s . with the o b j e c ­
tives of:
growth
(I) D e t e r m i n a t i o n of pathogen virulence and
alterations in response to diclofop exposure, (2)
Evaluation of diclofop and pathogen interactions in wheat
under field conditions, (3) Investigation of wheat root
responses to diclofop in the presence and absence of G.
graminis
6
LITERATURE REVIEW
Herbicide»Pathogen Interactions
The first selective herbicide developed for use in
agronomic crops was 2,4-dichlorophenoxy acetic acid (2,4D ).
This
ne w
management
American farmers in 1945.
tool
became
available
to
Since the introduction of 2,4-
D , selective herbicides have become an integral part of
modern agriculture. With the development of herbicides
that
alter the growth of higher plants,
interest
in their effects
came a parallel
on other organisms,
including
plant pathogens. As early as 1947 Fenner and Fate (1947)
reported
that
2,4-D treatment
of. Ceratocvstis u l m i . the
causal agent of Dutch Elm Disease, caused the formation
of
a bnormally
large
and
misshapen
coremial
masses.
Richards (1949) reported that 2,4-D and 2,4,5-T (2,4,5trichlorophenoxy acetic acid) caused irregularities in
mycelial
growth
and spore germination of several
fungal
pathogens when grown on herbicide amended media. However,
the application of 2,4-D or 2,4,5-T to crop plants did
not necessarily affect disease development.
study
that
conducted
2,4-D
incidence
by Sackston (1948),
applications
or
severity
to flax
it was determined
had
o f disease
In a field
no effect
caused
by
on the
Seotoria
7
linicola or Melamnsora Iini.
As
continued
research
led
to
the
development
of
various classes of herbicides, the study of the effects
of
these
ne w
widespread.
materials
Herbicide
on
plant
interactions
pathdgens
with
plant
became
pathogens
are expressed as effecting an i n c r e a s e , decrease or no
change
in
plant
proposed
thr e e
influence
disease.
mechanisms
disease
inhibitory
or
Katan
and
by
which
development.
stimulatory
Eshel
have
herbicides
These
effects
(1973)
include
on
the
can
direct
pathogen,
changes in host susceptability and alterations in c o m ­
petitive
interactions.
Direct effects of herbicides on pathogens are best
studied
in the laboratory.
of herbicides
There
herbicide,
studied.
Many
examples
causing changes in the growth and develop­
ment of pathogenic organisms.
the
are numerous
its
These effects vary with
concentration,
of these
studies
have
and
been
the
organism
reviewed
by
Katan and Eshel (1973) as well as by Altman and Campbell
(1977).
Katan and Eshel (1972) have postulated that h e r b i ­
cides could effect
pathogen virulence by altering fungal
metabolism or growth.
However, experimental evidence of
8
herbicide
induced
limited.
(1951)
changes
in
pathogen
virulence
is
An inconclusive report by Hsia and Christensen
found
that
virulence
of Helminthosnorium
sativum
on wheat increased when the fungus was cultured on media
containing 2,4-D.
However, changes in disease severity
could have been the result of direct effects of 2,4-D in
small
amounts
on
the
host,
rather
than on herbicide-
induced changes in the pathogen.
The
mechanisms
of
action
of herbicides
p a t h o g e n s .may be similar to those operative
plants.
Membrane
of
membrane
integrity
of
several
fungi.
disruption caused by peroxidation of lipids has
shown
to be
paraquat's
mechanism
higher plants (Hatzios and Pfenner^
Host
susceptibility
treatment.
Herbicides
ological
traits
pathogen
interactions
1973,
in higher
Sahid and Lyon (1981) showed that paraquat caused
disruption
been
on plant
Davis
and
respiration,
cell
be
action in
1982).
changed
by
herbicide
may alter morphological and physi­
in host plants which can affect host(Altman,
Dimond,
effects on cell division,
production,
can
of
wall
1956).
Katan
These
and E s h e l ,
may
meristematic activity,
thickness,
metabolism,
1977,
as well
membrane
include
cuticle
permeability,
as other plant charac­
teristics and functions (Hatzios and Pfenner, 1982).
9
Alterations
in
competitive
interactions
indirectly affect the pathogen. Understandably,
may
organisms
vq.ry in their ability to metabolize herbicides (Wilkinson
and
L u c a s , 196 9b;
herbicide
could
Kurt?
change
et
al., 1982).
Therefore,
a
the population of pathogens by
favoring the development
of one organism over the other.
Such changes occur when
the herbicide is more toxic to
some
population
members
th e
interactions
disease are complex.
increase
in
laboratory
than
1982 ; Wilkinson and Lucas,
(Cerkauskas,
The
of
plant
between
Although
disease
condition?,
to
1969a,b).
herbicides
a change
may
oth e r s
be
and
leading to an
observed
a corresponding
plant
response
und e r
may not
nepessarily be observed in the field. Although Johnston
et al. ( 1980 ) fovind that in greenhouse studies several
dinitroanaline
herbicides
could, reduce
in peas caused by a Fusarium complex,
support
these findings.
disease
severity
field data did not
In the field neither reductions
in pea yield nor root rot severity where observed.
Timing
outcome
of
of
herbicide
pathogen
application may
interactions.
influence
Richardson
the
(1959)
found that 2,4-D applied to sand seven days before inocu­
lation
of
ivcopersioii
tomatoes
decreased
with
wilt,
Fusarium
whereas
oxvsporum
applications
JLt
after
IO
inoculation
also
increased
affect
the
disease severity.
interactions
between
Soil type may
herbicides
and
pathogens. Filo and Dhingra (1980) found that in a sandy
clay
loam
soil
M^rnnhomina
d lnoseb
reduced
phaseolifliL by 96*,
populations
of
whereas in a sandy loam
populations were reduced by 61*. Differences in disease
interactions that vary with soil type are perhaps related
to
th e
herbicide
characteristics
reaction
soil
types
the
soil.
as binding to soil colloids,
pH reaction, and volatility
of soil borne
in
pathogens
(New m a n
Such
solubility,
can influence the exposure
to the herbicide in different
end Downing,
1958;
Regardless of the means of application,
eventually reach the soil.
Therefore,
Altman;
1977).
all herbicides
an organism living
in the soil
is likely to be influenced by a herbicide.
Research
soil-borne
on
diseases
has
been
extensive,
increases as well as decreases in disease severity have
been documented.
Hsia
and
Christensen
increased
the
incidence
caused
by
nthosnorium
(1951)
of
showed
seedling
gaU.
VJim.
that
blight
of
They concluded
2,4-D
wheat
that
the increase in disease was due to an increase in host
susceptibility caused by herbicide application.
Richardson (1957) found that 2,4-D,
However,
^s- well as monuron
Tl
and dalapon,
herbicides
disease
found
reduced root rot infection in wheat.
studied,
severity.
no
only
maleic
hydrazide
Conversely, Tinline
correlation
between
phenoxy
Of the
increased
and Hunter
herbicide
(1982)
applica­
tion and the incidence or severity of common root rot in
wheat. In laboratory studies Hodges (1977, 1981) showed
that
2,4-D
could
increase
Helminthosporium
mycelial growth and conidiospore germination.
reference
was made to seedling diseases,
sativum
Although no
Hodges found
that leaf spot caused by jL. sativum was increased due to
foliar applications of 2,4-D in turfgrass (Hodges,
Madson
and
Hodges
(1982)
found
that
MCPP,
1977).
a phenoxy
herbicide similar in mode of action to 2,4-D, decreased
the
content
plants.
of
sucrose
and
soluble
sugars
in
treated
The low sugar levels were correlated with an
increase of Hujl sativum leaf spot.
Increases
increase
Altman
the
(1972)
cycloate
in
root
exudation
incidence
showed
increased
of
that
damping
some
in
have
been
soil-borne
sugarbeets
off
caused
by
shown
to
diseases.
pyrazon
and
Rhizoctonia
solani by 50%. An increase in glucpse exudate from herbi­
cide treated roots caused increased sclerotia germination
in the rhizosphere, which led to increased damping-off.
Similarly
Lee
and Lockwood
(1977)
found
that
chloramben
enhanced soybean dampi n g - o f f caused
MsjLaS-La..
In
the
field,
plant
by Thielavionsia
stand
and
yield
were
reduced when c hloramben was applied to infested soils.
Laboratory
basicola
exper i m e n t s
spores
rhizospheres
was
showed
two
of treated
to
that g e r m i n a t i o n
four
times
higher
soybean seedlings.
of T.
in the
Herbicide
induced root exudatiop of amino acids stimulated spore
germination
which
led to an increase in soybean disease
severity.
Changes
cide
in inoculum potential as a result of herbi­
application
Etnd Campbell,
can
affect
1977).
disease
development
Duncan and Paxton (1981)
although Phytophthora m e e a s o e r m a var.
culture
was
inhibited
production
was
by trifluralin,
observed.
(Altman
found that
so iae grow t h in
increased
oospore
It was theorized that an in ­
crease in oospore production may lead to the increase in
Phytophthora
beans.
root
Nilsson
increased
rot
(1973a)
perithecia
Gaeumannomvces
noted
in trifluhalin
found
and
craminis
that
MCPP
microspore
in culture.
treated
soy­
(mecroprop)
production
of
Such changes may.
account for the increases in Take-AlI disease observed in
wheat fields treated with MCPP (Nilsson,
Herbicides may
of
plant
pathogens
indirectly
in the
influence
soil.
1973b).
the populations
Wilkinson
and
Lucas
13
(1969a) showed that herbicide residues in plant tissues
can affect competition among fungi.
quat
In their study para­
treated tissues were more condusive to colonization
by Fusarium culmorum than by Trichoderma viride. Similar
results
were
found
for
Rhizo pus
stolonifer
and
Aspergillus niger. Therefore herbicide treatment may lead
to
increases or decreases in plant disease by changing
the competitive ability of plant pathogens.
The Herbicide Diclofop-methvl
D i c l o f op-methyl
oxy)phenoxy)
(methyl
2-(4-( 2', 4 ’- dichlorophen-
panoate), hereafter referred to as diclofop,
is a diphenyl-ethpr herbicide that has both preemergence
and
post
plants
emergence, activity.
include
restricted
Symptoms
c h l o r o s i s , necrosis,
root growth.
on susceptible
stunting,
and
The herbicide can be absorbed
through the foliage as well as through the roots.
Both
sensitive and tolerant species absorb significant amounts
of herbicide (Boldt and P u t n a m , 1980), however, sus c e p ­
tible
species are unable to detoxify the herbicide while
tolerant
species
(Shimabukuro
et
Although,
inactivate the herbicide metabolically
aT., 197 9) •
the specific mechanism of activity is not
fully understood,
Boldt
and Putnam
(1980,
1981)
noted
14
irregularities
in
chlorophyll
content
and phloem
trans­
port as well as changes in the rates of photosynthesis
and ATP production.
auxin
antagonism
whereas
Brezeanu
(197 9) ,
and
changes
in
Shimabukuro
as
a primary
et al.
mechanism
et
al.
(1976),
Crowley
and
P r e n d e v i lie
membrane
integrity
(1978)
Davis
which
implicated
of. activity,
and
Brezeanu
(1979)
observed
may
be
directly
related to cell death leading to plant dysfunction.
As related to soil-borne disease, perhaps the most
interesting
aspect
of diclofop activity in
decreased root growth.
plants is
Root pruning has been observe^ in
susceptible as well as in tolerant plants. In tolerant
plants root pruning is more pronounced when soils are wet
and temperatures are cool. Under such conditions roots
may absorb more herbicide due to increased root exposure
because
wet
conditions
may concentrate
the herbicide in
the soil water around the root zone. Low temperatures may
decrease
the p l a n t ’s metabolic
r a t e , thereby reducing
detoxification and increasing the concentration of the
active herbicide in the tissue.
Chow
and LaBerge (1978)
suggested that root pruning
is the result of a decrease in t ransportation of photosynthate
effect
from the leaves,
on
the
root.
In
rather than from
more
recent
any direct
investigations,
t
^orrison et al. (198 1) measured differences in wheat root
growth
with
root
exposure
to diclofop.
were obtained by Donald et al. (1982).
Similar results
In these studies
reduction in adventitious root initiation as well as root
length were detected.
Histological
Morrison et al. (1981) indicate
division
in
interphase.
roots
prior
to
studies conducted by
that diclofop stops cell
mitosis,
possibly
during
Within roots, other effects included tissue
disruption in the central cylinder and structural deteri­
oration of the epidermis.
Changes
in root
growth
and morphology
may
wheat susceptibility to root infecting pathogens.
by Nilsson (1973a)
the herbicide
increase
A study
suggested that wheat roots damaged by
MCPP (Mecroprop)
were more easily pe n e ­
trated by C a e u m a n n o m v c e s c r a m i n i s .
The roots in these
studies were stunted and had bulbous tips due to her b i ­
cide application.
Similar symptoms are seen with diclofop
Morrison et al., I 98I), .however the
(Donald et al., 1982;
result of these changes on disease incidence or severity
have not been investigated.
Aside from field observations,
controlled
studies
conducted
diclofop interactions.
affect
of diclofop
In fact
on plant
on
there have been no
wheat
diseases
and
the only research on the
disease
was
conducted by
16
Ruppel et al. ( 1 982).
In a sugarbeet field t r i a l , they
found no significant interactions between diclofop and
Rhizoctonia
solani.
17
MATERIALS AND METHODS
The Pathogens
The
pathogenic
isolates
of R 1- s o r o k i n i a n a . R jl
o u l m o r u m . G. gram i n i s , and CL, g r a m i n e u m were obtained
from D.E. Mat h r e , Plant Pathology D e p a r t m e n t , Montana
State University,
Bozeman,
Mont a n a 59715. The isolates
used in this research were Bj. sorokiniana isolate 21M and
F . culmorum
Isolate 20 9. ILl g raminis and CL. g ram i n e u m
were isolations from infected wheat grown in Montana.
All isolates were highly virulent.
Field studies w ith Cenhalosporium gramineum
Ce p h a l o s p o r i u m
Bozeman,
Montana
Research
Field
field
at
the
Laboratory
trials
Arthur
and
were
H.
established
Post
at; the
Researph Center at Moccasin,
the
1981.
fall
of
Three
winter
Agricultural
Central
Agricultural
wheat
in
Montana
Montana during
cultivars
witty
differential susceptibility to Cephalosporium stripe were
seeded.
These
13670),
both
17902),
were
Reflwin (Cl
susceptible
17 84 4) and
cultivars,
and
Winalta
(Cl
Winridge
(Cl
a cultivar with only moderate susceptibility.
To
insure uniform disease development the plots were inocu­
lated at planting with oat kernel inoculum at the rate of
I
18
1.5 grams per meter of row (Mathre and Johnston,
Plots
were
seeded
in Moccasin
on September
1975).
11 and on
September 17 in Bozeman using a cone-seeder. The seed and
inoculum were added simultaneously to the row.
Treatments were arranged in a split plot design with
four replications.
block.
Plots
Each of the cultivars was seeded in a
consisted
of 12 rows
with lengths of 3-3
meters at Bozeman, and it.5 meters at Moccasin. I n o c u l a ­
tions were split with six rows inoculated and six rows
uninoculated.
Diclofop
was applied to 12 row plots at
rates of 0, 1.12 and 2.24 kg. ai per HA.
All treatments
were randomized within a block design.
Diclofop
application,
(Tottman,
was
applied
in
the
spring
wheat was fully tillered,
et al. 1 97 9).
of
1982.
At
Zadoks stage 2lf
Herbicide applications were made
with a backpack sprayer calibrated to deliver 76 1/HA at
a pressure of 2.39 k g / cm2.
weeds
were
controlled
At both locations broadleaf
with
Bronate
(MCPA
plus
oxynil). To avoid d i c l o f op-phenoxy antagonism,
brom-
Bronate
was applied to all plots 15 to 20 days after the diclofpp
applications.
Herbicide
diclofop
No other pesticides were applied.
injury
applications,
ratings
were mg.de 14 days after
Phytotoxicity ratings were based
on visual e s t i m a t i o n of percent stunting and degree of
lea f
yellowing.
considered
A
rating
commercially
of
ov e r
20?
unacceptable, while
100? indicated all plants dead.
Additionally,
rated
a visual
for
percentage
disease
white
severity
heads
by
per plot.
injury
was
a rating of
plots were
estim a t i o n of
These evaluations
were
made after flowering when the white heads were clearly
evident.
At Moccasin,
prior to harvest,
mowing 0.3 meters from each end.
each six row plot
rows were trimmed by
The center four rows of
were harvested frith a plot combine.
The grain was weighed and yields recorded. At Bozeman,
2.5 meters of row were hand harvested from th^ middle pf
each of the center t>fo rpws.
The hea,<^s were threshed end
cleaned mechanically. The grain was weighed and yields
recorded.
Field
Studies
with
Fusarium
culmorum
and
B i n o l aris
sorokiniana
Field trials were established in the spring of 1982
at Bozeman,
Montana on the Arthur H. Post Agricultural
Research Field Laboratory,
Agricultural
and at thp Central
Reseach Center at
Mopcasin,
Montana.
1983 the experiment was repeated at Moccasin.
design was used for all tests.
wheat
(Cl 13596)
Montana
In
%h# same
Plots of Fortuna spring
were artifically inoculated with either
20
B. aorokiniana or PL. culmorum
using oat kernel inoculum.
The procedure for making the inoculum was similar to
that
outlined
by
Mathre
and
Johnston
(1975)
gramineum. Inoculum for field trials was.made
ing
aorokiniana
kernels.
In
and Z i. c u l m o r u m
by cultur­
on autoclaved
oat
I liter glass jars were placed 15 0 grams
oats with 100 ml distilled water.
Whatman
for IL.
qualitative
filter
Jars were covered with
paper,
7.0 dm- in diameter.
Metal lids with a 12 mm diameter hole in the center were
then screwed onto the jars.
121 C for 20 minutes.
The oats were autoclaved at
After autoclaving the oats were
allowed to cool at 21 C for 24 hours.
After cooling,
8
mycelial plugs I cm in diameter were placed in each jar.
Mycelial
plugs
were
taken
from IL_ sorokiniana
culmorum
cultures growing on potato dextrose
and £*.
agar.
Jars
were shaken to distribute the mycelial plugs ,among the
oat kernels.
The oats were incubated three weeks at 21
C. After three weeks,
mycelia,
the
when the oats were well covered by
oat kernels were
removed
from
the jars,
spread on sheets of brown paper, and allowed to air dry
at 21 C .
After drying the inoculum was placed in paper
sacks and stored at 5 C until used.
The inoculum was applied simultaneously
with the
seed at planting at a rate of three grams inoculum per
21
meter
of
row.
A cone-seeder
was
used
for
planting.
Treatments were arranged in a split plot design with four
replications.
Plots consisted of 12 rows with lengths of
3*3 meters at Bozeman and 6 meters at Moccasin.
Inocula­
tions were split with six rows inoculated and six rows
uninoculated.
Diclofop was applied to 12 row plots at
rates of 0, 1.12 and 2.24 kg. ai/HA.
FL. c u l m o r u m
treat m e n t s
were
sorokiniana and
in separate
blocks.
All
treatments within the block were randomized.
Diclofop
was
applied
to
tillering
w h e a t , Zadoks
stage 22. Herbicide applications were made with a b a c k ­
pack sprayer calibrated to deliver 76 1/HA at a pressure
of 2.39 k g / c m ^ . in all tests,
Bronate (MCPA plus brom-
oxynil) was applied for broadleaf weed control.
d i c l o f op-phenoxy antagonism,
made
1 5 to 26 days
To avoid
Bronate applications were
after the diclofop application.
No
other pesticides were used.
Herbicide
injury
diclofop application.
visual
estimation
yellowing.
all
were
made
14 days after
Phytotoxicity ratings were based on
of
percent
stunting
and
degree
of
A rating of 20% injury was considered to be
commercially
cated
ratings
unacceptable, while
plants
were
dead.
a rating of 100% indi­
To estimate
the combined
effects of disease and herbicide on crop vigor,
a visual
22
assessment
;
•
including height and stand
of percent injury,
reductions,
was made at harvest.
Yield data were col­
lected following the procedure outlined for .£*_ gramineum
field
plots.
As
an
internode
indication
ratings
sorokiniana
wheat
of
disease
from
counted at harvest.
0.3
plots.
meters
of
row
these
were
ratings
pulled
and
was rated for degree of necrosis.
A scale of 0 to 3 was used.
A rating of 0 represented
tissue without lesions;
p r e s e n t , however,
For
The sample was taken from row three.
The subcrown internode
healthy
subcrown
and stand counts were taken from B .
and F_&. c u l m o r u m
plants
severity,
I represented lesions
not coalescing^ around the internode
tissue; 2 represented lesions coalescing but with no more
than 50% necrosis;
greater
3 represented lesions coalescing with
than 50% necrosis.
As an inoculum control, prepared
oat kernel inocu­
lum was autoclaved to destroy the fungi.
This autoclaved
inoculum was added to row four in the uninoculated con­
trol
plots.
also
3 grams
The rate fpr the autoclaved inoculum was
per
meter
of
row.
At
sampling
disease
ratings from rows three and four were compared.
Field Studies with Gaeumannomvces graminis
Field trials were established at the same locations
23
as CL. g r a m i n e u m field trials. Fortuna spring wheat was
artifically inoculated using oat kernal inoculum.. A rate
of 1.6 grams of inoculum per meter of row was applied at
planting.
were
The e x perimental design and plot treatment
identical
to that given,in the above section for
Fusarium and Bipolaris.
Greenhouse Studies with Gaeumannomvces graminis
Surface sterilized wheat s e e d s , cultivar Butte (Cl
17681),
tic
were incubated seven to ten days;at 21 C in plas­
boxes
lined
sterilized
with
paper
toweling.
Seeds
we r e
by soaking for five minutes in 0.5% sodium
hypochlorite. The seedlings were transferred to I liter
opaque.glass culture jars containing one-half strength
Hoagland’s solution,
when the leaf reached thfe eoleoptile
tip, Zadoks stage 09. Styrofoam corks with holes for each
seedling
were
used
to
cover
the
jars
ap,d support
the
seedlings. Each jar contained two seedlings.
The
seedlings were maint a i n e d in the greenhouse.
The day length
mentary
during
days
was extended to 14 hours using supple­
fluorescent lighting.
the night
the
strength
chelated
and 24 C during
nutrient
solution
Hoagland's
iron.
The
Temperatures averaged 8 C
was
solution
nutrient
the day.
After seven
replaced
enriched
solution was
with
with
changed
full
4 mg/1
weekly
24
for the duration of the experiment.
Additional nutrient
solution was added as needed to maintain the liquid in
the culture jars at I liter.
The nutrient solution was
continuously aerated with compressed air.
When the seedlings reached two leaves,
Zadoks stage
12, 50% of them were inoculated with IL. eraminis.
lation
was
a c c omplished
Inocu­
by attaching a' I cm diameter
mycelial plug to the shoot just above the seed.
Mycelial
plugs were removed from Gj. eraminis cultures grown on
PDA.
These plugs were attached to the seedling by wrap­
ping
them
to the plant with moistened cotton strands.
The inoculum was positioned just above the liquid in the
culture
jars.
At tillering, Zadoks stage 22, the wheat was treated
with diclofop to reach a final concentration of 3 uM for
48
hours.
culture
jars.
The
herbicide
According
was
added
directly
to Shimabukuro
(1982),
to
the
a 3 uM
diclofop solution will alter wheat root growth with a 48
hour exposure time. After 48 hours the solutions in all
the
culture
jars
were
replaced
with
fresh
H o a g l a n d 's
solution.
Treatments
consisted
graminis. diclofop,
of
an
untreated
check,
G.
and Uj. graminis plus diclofop. Treat­
ments consisted of eight
plants,
planted two plants per
25
jar.
The jars were arranged on the greenhouse bench in a
completely randomized design.
At heading, Zadoks stage 59, roots were clipped from
the plants.
Secondary root length was evaluated by aver­
aging the root length of the uppermost five roots.
root volume
root
mass
was measured
in
a kno w n
Live
volumetrically by emersing the
volume
of
change in volume of the water.
water
and
noting
the
The .roots were then oven
dried at 55 C for 24 hours and weighed.
Analysis of variance
among
treatments.
was used to detect differences
Compa r i s o n s
among means
were made
using Student Newman Keuls test (SNK) for equal means.
Studies on the Fungitoxicitv of Diclofon
The
effect
of
diclofop
on
the
growth
of
B.
s o r o k i n i a n a . F . o u l m o r u m , CL. grami neum , and £Ll. graminis
was
evaluated
amended
by
potato
culturing
dextrose
prepared as directed.
these
aga r
fungi
(PDA).
on
dic l o f op-
Difco
PDA. was
The autoclaved PDA was cooled to
45 C. A c o m m e r c i a l diclofop formul a t i o n containing 360
grams
per liter diclofop was then added to the PDA to
produce amended PDA with diclofop concentrations of 0, I ,
10,
100,
and
1,000
mg/1.
Amended
PDA was
poured
into
plastic Petri plates and cooled.
To compare
the effects of the solvents,
surfactants
26
and
other
compounds
formulation,
found
in the commerc'ial
a blank formulation
containing
diclofop
no diclofop
was compared to the formulated herbicide at volumes equal
to those required to produce I, 10 , 100 , and 1,000 m g /1
concentrations
of
diclofop.
Both
the commercial
herbi­
cide and the blank formulation were supplied by American
Hoechst
Corporation,
Somerville,
NJ.
All fungi were maintained on PDA. A 10 m m mycelial
plug taken from the outer edge of an actively-growing
culture
was
placed
in the
center
containing PDA or amended PDA.
fungus
were
taken
from
of each
Petri, plate
All transfers for each
the same
culture
plate.
Each
treatment was replicated five times.
Culture
plates
were
maintained
at 21
C.
Radial
mycelial growth was measured when the mycelia in one of
the treatments reached the edge of the Petri plate. A two
factor analysis of variance was used to determine differ­
ences
among
treatments.
Treatment
means
were
compared
using an LSD at the 5% level.
Studies on Diclofop Induced Virulence Changes
To
determine
if diclofop
exposure
produces
physio­
logical or genetic changes within the pathogens that may
alter virulence, virulence tests were conducted.
mycelial plug was taken from cultures of
A 10 mm
cramineum. B.
27
j
: ■
sorokiniana. G. graminis. and Fj. Gulmorum growing on PDA
amended with 100 mg/1 diclofop.
ferred to PDA.
The plugs were trans­
This transfer was done to eliminate the
effects of diclofop contained in the amended media on the
wheat.
Simultaneously, a mycelial plug from an unamended
PDA culture of the same age was transferred to PDA.
The cultures of all but Cj_ gramineum were incubated
10 days at 21 C.
After incubation a 22 mm mycelial plug
was cut from the media and placed in a C o n e - tainer 3 cm
in diameter, which had been filled with moistened vermiculite.
scale
Pre-germinated Butte
05,
wheat
seeds,
were placed on top of the mycelial
covered with vermiculite.
exposed
spring
to diclofop,
were also included.
Zadoks
plug and
Controls from cultures not
as well as uninoculated
Each treatment
controls
was replicated 10
times.
In the case of Cj. gramineum
bated
the cultures were incu­
26 days at 21 C , to allow for adequate mycelial
growth.
After incubation eight 10 mm mycelial plugs were
mixed with sufficient moistened vermiculite to fill a 10
cm pot.
Two Butte spring wheat plants at the one node
stage, Zadoks scale 30, were placed in each pot.
Prior
to transplanting seedlings had been grown in vermiculite.
In order to facilitate infection the wheat root mass was
28
t r i m m e d to I 2 cm at transplanting.
A control from cu l ­
tures not exposed to diclofop was included, as well as an
uninoculated control.
times
with
two
Treatments were replicated four
plants
per p o t , i.e.
eight
plants
per
treatment.
The Cone-tainers
greenhouse,
and pots
were m a intained
in the
with day temperatures of 18 C and night tem­
peratures of 8 C. Plants were fertilized as needed with
full
strength Hoagland’s solution.
At four weeks after inoculation each plant was rated
for disease severity.
with
0 representing
complete
A rating scale of 0 to 5 was used
healthy,
leaf necrosis.
and with 5 representing
With iLu gramineumr plant height
was measured and leaf striping noted.
29
RESULTS
Field Studies with Cephalosporium gramlneum
The
application of diclofop to winter wheat had no
effect on yield of either Cjl. sramineum infected plants or
healthy
plants.
ferences
However,
between
significant
infected
at both locations (Table
and healthy
I).
(P<0.05)
plants
no herbicide
tion,
this
trend
and decreased
was
not
differ­
was greatest
with herbicide
statistically
dif­
were found
Although the yield
ence betw e e n healthy and infected wheat
with
yield
applica­
significant
(P<0.05) (Table 2 ). An analysis of variance was used to
compare
treatments.
No significant differences in other
parameters were found.
Neither visual disease assessment
or visual herbicide injury assessment showed any differ­
ence in reaction bet w e e n healthy and diseased wheat to
diclofop.
30
Table I .
Effect of Cephalosporium gramineum on yield of
three winter wheat cultivars at B o z e m a n and
Moccasin, Montana in 1982.
Yield (kg/EA) 1
Winalta 2
Mean
Redwin 2
Winridge 2
Uninoculated
3703 a
44448
S77I a
3973a
Inoculated
2896b
3367b
2963^
3097b
Inoculation
I Averaged across 0, 1.12, and 2.2M kg ai/HA dielofop.
^yields
are the mean of 4 .replications at 2 locations;
values in the same column are different when followed by
different letters, LSD at 5%•
Table 2.
Effect of d i c l o f o p-methyl on yield of winter
wheat uninoculated or inoculated with .Csph&.lo=
snorium gramineaum.
Yield (kg/HA)1’ 2
Diclofop-methyl
(kg ai/HA)
Difference
0.0
3990a
2 92 9a
1061s
1.12
4027s
3178s
2.24
3 87 9a
849a '
to
CO
Inoculated
U)
Uninoculated
1Yields
are a mean of 4 replications at
averaged across 3 cultivars.
761s
2
locations,
^Values in the same column are different when followed by
different letters, LSD at 5%•
31
Field
Studies
with
Fusarium
culmorum; and
Bioolaris
sorokiniana.
Dryland
root rot field trials over
three
location
years indicated that wheat in both inoculated and uninoc­
ulated
Yield
gens
1 982,
plots responded similarly to diclofop
treatment.
decreases due to inoculation with these two patho­
were significant (P<0.05),
for
jL.
sorokiniana
in
and for Fj. culmorum in 1 983. These yield responses
were significant only at Moccasin.
Otherwise, inoculation
with these two pathogens caused no effect on yield (Table
3) .
Table 3 .
Effect
of Bipolaris sorokiniana or Fusarium
culmorum inoculation on yield of Fortune spring
wheat
at Moccasin
(Me)
and Bozeman
(Bz),
Montana.2
Yield (kg/HA)1 ’ 2
Inoculum
Added
Bj. sorokiniana
I 982
1983
Mc
Bz
Mo
F . culmorum
1 9821 983
Mc
Bz
MC
No
I46 8a
3113 a
224 9a
1297*
331 1*
2269*
Yes
I257b
3125 a
221 Ia
I 246a
3266 a
2215b
1Yields are a mean of 4 replications averaged across
1.12 and 2.24 Kg ai/HA diclofopv
0,
2Values in the same column are different when followed by
different letters, LSD at 5% level.
32
When comparing plots inoculated witjh EJ culmorum to
non-inoculated
(P<0.05)
plots,
between
no
diclofop
significant
application
detected (Table 4).
However,
in inoculated
increased
diclofop
plots.
plots
applications,
Herbicide
and
yield
were
with IL. sorokiniana. yields
when
induced
interactions
significantly
compared
yield
(P<0.1)
with
to uninoculated
increases
in inoculated
plots were noted at both Moccasin and B o z e m a n in 1982,
but no interactions were detected in 1 983 (Table. 5).1
2
Table 4.
Diclofop
(kg ai/HA)
O
O
1.12
Effect of d i c l o f o p-methyl on yield of Fortqna
spring wheat uninoculated (U) or inoculated (I)
with Fusarium culmorum.
Yield (kg/HA)1 ’ 2
I 982
I 983
Bozeman
U
I
Moccasin
U
I
Moccasin
U
I
CU
OJ
1374a
I253a
3717*
3 13 1a
2303*
2256a
I 205a
11 85a
305 1a
3252a
231Oa
2208a
13 I3a
IBOOa
3 I6 5a
34 14a
21 95a
21 82a
1Yields are mean of 4 replications.
i
2Values in the same column are different when followed by
different letters, LSD at 5$.
33
Table 5.
Effects of diclofop-methyl on yield of Fortune
spring wheat uninoculated (U) or inoculated (I)
with Bipolaris sorokiniana .
Diclofopmethyl
(kg ai/HA)1
2
Yield (kg/HA) 1 ’ 2
I 982
1983
Bozeman
U
I
Moccasin
U
I
Moccasin
U
I
2.24
I441 a
2842*
226 9*
2155*
3138*
3508^
2242*
2249*
1515^
2842*
3024b
2236*
2229*
CM
I 542a
3360*
<ti
1.12
1044*
CM
O
O
I421 &
'
1Yields are a mean of 4 replications.
2
tValues in the same column are different when followed by
different letters, LSD at 5%.
For
EU. .sorokiniana
at B o z e m a n
in
1 982 d i s e a s e
ratings based on subcrown internode necrosis,
showed that
disease severity was greater in the inoculated plots than
in
the
levels
uninoculated
of
plots
( P < 0.1 ).
B,^ s o r o k i n i a n a . no
Due
differences
severity were noted at Moccasin (Table 6 ).
difference
in
subcrown
internode
to
background
in
disease
There was no
ratings between
plants
in rows with autoclaved inoculum compared to uninoculated
rows
(P<0.1).
both locations
Wheat
stand was reduced by inoculation at
(Table 6 ).
r
34
Table 6 .
Effects of Bioolaris sorokiniana inoculation on
percent disease (D)^, percent severe disease
(SD)2 , and wheat population (P) and yield at
Bozeman and Moccasin, Montana in 1982;^’ 4
Bozeman
% SD
P
Moccasin
SD
P
D
%
&
on
w
■t—
Inoculated
I .4b
.0.5b
I9.9 b
Uninoculated
8.5a
5 .Oa
6 .7 a
I
%
5.Ia , I .5 a
0 .7 a
3 •5a
cr
D
IN)
O
%
Percent
disease represents the percentage
of subcrown
internodes with lesions and/or some degree of necrosis.
p
Percent
severe
disease
represents the percentage
subcrown
internodes with coalescing lesions and 5 0 %
greater subcrown internode necrosis. .
of
or
^Values represent an average of 4 replications,
based on
0.3 peter row sample, averaged across 0, 1.12, and 2.24
kg ai/HA diclofop.
^Numbers in the same column are different when
by different letters, LSD at 5 % .
For
culmorum
in 1982 disease
followed
ratings
based on
subcrown internode necrosis showed that at both locations
a greater number of plants were severely infected
in
inoculated plots compared to uninoculated plots (Table
7 ).
The difference
inoculated
Bozeman
and
in percent overall infection between
uninoculated
(P < 0.0 5) , but
sorokiniana.
responsible
not
background
for
a lack
plots
at
levels
of
was
significant
Moccasin.
of
response
As
with
culmorum
at
B.
were
to inoculation
in
35
overall disease rating.
to inoculation
was noted
A reduction in wheat stand due
at B o z e m a n (Table 7).
There
were no differences in subcrown internode ratings between
plants in rows with autoclaved inoculum compared to unin­
oculated
rows
Table 7 •
(P<0.1).
Effects of Fusarium c u l m o r u m inoculation on
percent disease (D)^, percent severe disease
(SD) and wheat population (P) at B o z e m a n and
Moccasin, Montana in 1982 .3 » %
P
%
Moccasin
% SD
D
P
Inoculated
50.4a
4.7 a
16 a
3 4.18a
2.9a
ro
0
Ul
o>
%
Bozeman
% SD
D
Uninoculated
30.3^
2.4b
I 9b
31 .4la
I .4b
21 .3a
1
Percent
disease represents the percentage
of subcrown
internodes with lesions and/or some degree of necrosis.
2
Percent
s.evere disease
represents the percentage
subcrown
internodes with coalescing lesions and 5 0 %
greater subcrown internode necrosis.
of
or
3Values represent an averge of 4 replications, based on
0.3 meter row sample, averged across 0 , 1.12 and 2.24 kg
ai/HA diclofopi
^Numbers
in the same column are different when
by different letters, LSD at 5 % •
followed
No visual herbicide injury was noted at the 1.12 kg
ai/HA r a t e , either I 4 days after application or at ha r ­
vest.
However,
at 2.24 kg ai/HA,
wheat injury of 15 % was
36
observed 14 days after application at bioth !locations in
1982.
No injury was noted in 1983.
No differences were
apparent in degree of visual injury between inoculated
and uninoculated plots.
Field Studies with Gaeumannomvces gram inis
Inoculum
density
and
favorable
moisture
combined to reduce stands of Fortuna wheat by
to severe disease losses no herbicide-G.
actions could be evaluated.
conditions
90%.
Due
graminis inter­
Similar tests in 1983 were
destroyed by hail and animal grazing.
Greenhouse Studies with Gaeumannomvces graminis
In a
healthy
8 ).
hydroponic system, diclofop applications to
wheat
reduced
Conversely,
root
diclofop
volume
and dry weight (Table
applications
to XL. graminis
infected wheat caused no differences in root volume or
dry weight (Table 8 ).
to
diclofop
were
diseased roots,
cant
(PC0.05)
more
Since responses of healthy roots
pronounced
than
were
those
of
an analysis of variance detected signifi­
interactions between
graminis
infection
and diclofop treatment (Figure I). These data indicate
that the effect of diclofop on root volume and dry weight
is less severe in diseased wheat than in healthy wheat. A
significant
reduction
in root
length
due
to
diclofop
37
treatment wap noted in both infected and healthy wheat
(Table
8 ).
Both diseased
and healthy
roots responded
similarly to diclofop in respect to root growth reduction
(Figure 2 ).
TABLE 8 .
Effects of treatment with d i d o fop-methyl on
root v o l u m e , dry weight and length of Butte
Spring wheat, with or without G a e u m a n n o m v c e s
graminis inoculation.I
Wheat Root Response 2
No Inoculation
DiclofopMethyl
Concentration
With Inoculation
Vol
(cc)
Wt
(mg)
Length
(mm)
Vol
(cc)
Wt
(mg)
Length
(mm)
0 uM
5 .Ita
275a
13.8a
I .9a
7 Oa
I I.Oa
3 uM
2.5b
IIBb
8.7 b
I .5a
7 9a
6.5b
IValues in the same column are different when followed by
different
letters.
Student
Newman Keuls test
at 5%
level.
p
Average of 8 replications with I plant per replicate.
Diclofop Fungitoxicitv Studies
At the concentrations evaluated,
pathogen growth except for
ulation
culmorum
was
noted
wa s
at
10
tolerant
diclofop inhibited
graminis where growth stim­
mg/1
to
( P< O.O 5)
diclo f o p .
(Table
9).
F.
Significant
F.
culmorum growth reductions were noted only at 1000 mg/ 1 .
38
Pathogen
growth
was
also
reduced
significantly
by
exposure to the herbicide formulation without diclofop
(P < 0.0 5) (Table 10).
Table 9 .
Effects of diclofop-methyl (DM) and dic l o f opmethyl formulation blank (PB) on radial growth
o f G a e u m a n n o m v c e s graminis. Cephalosporium
gramineum. Fusarlum c u l m o r u m . and Binolaris
sorokiniana.'
Growth (mm )1
2
Concentration
CL. gramineum
B . sorokiniana
F . culmorum
G . graminis
DM
FB
DM
FB
DM
FB
DM
O
75a
75a
7 8a
7 8a
7 8a
7 8a
64a
6 4a
I
70a
7 3a
66b
66 b
78a
76 a
6 I b
65a
I O
5 8b
7 2a
59c
71°
7 8a
7 8a
70°
65a
IO 2
38°
55b
36d
36d
77 a
64b
57d
46b
29d
36°
26a
29e
41b
IU c
13 e
I l c
O
UU
mg/1
FB
1Values represent an average of 5 replications.
2Values in the same column are different when followed by
different letters, LSD at 5$ level.
39
FIGURE I.
Changes in Root Volume (A.) and Dry Weight
(B.) in Response to Diclofop-Methyl in Healthy
versus Gaeumannomvces graminis Infected Butte
Spring Wheat.
A.
o
o
Healthy
Infected
CD
E
2
o
>
-*—»
O
O
DC
Diclofop Concentration
(uM)
B.
_
O)
E
■■■ Healthy
" " " Infected
-C
O)
*5
k.
Q
4—*
O
O
DC
Diclofop Concentration
(uM)
40
FIGURE 2.
C h a n g e s in A d v e n t i t i o u s Root L e n g t h In
Response to Diclofop-Methyl in Healthy versus
Gaeum annomvces graminis Infected Butte Spring
Wheat.
Healthy
Infected
Diclofop Concentration
(uM)
Table 10. Radial growth of Gaeumannomvces graminis (GG),
C e p h a l o s p o r i u m g r a m i n e u m (C G ) , F u s a r i u m
c u l m o r u m (FC), and Binolaris sorokiniana (RS)
on media amended with formulated d i c l o f opmethyl versus f o r m u l a t i o n additives without
diclofop-methyl .1
Growth (mm) 2
CG
BS
FC
GG
Formulation with diclofop
lt9a
ItTa
6 9a
5 1a
Formulation without diclofop
5 9b
51 b
66 b
47b
None
75°
78°
78 c
64°.
Media Additives
IValues are an average of 5 replications, averaged across
diclofop-methyl concentrations of 0 , I , 10 , 10^ and 10^
mg/ 1 .
2Values in the same column are different when followed by
different letters, LSD at 5/6 level.
Virulence Tests
An analysis of variance detected no changes in viru­
lence
( P < 0.0 5 ) of
£_«- e r a m i n i s . JVl
c u l m o r u m . JLl.
s o r o k i n i a n a . or C. g r a m i n e u m after exposure to 100 mg/1
diclofop.
Butte
spring wheat
was
susceptible
tion by all pathogens in this test (P<0.05).
to infec­
DISCUSSION
An increase in disease severity due to the direct
stimulatory effects of diclofop on Binolaris sorokiniana,
Fusarlum culmorum. Cephalosporium gramineum. or Gaeumannomyces graminis is unlikely.
Exposure studies and viru­
lence tests indicated that diclofop had no stimulatory
effect on grow t h rate or virulence of B . s o r o k i n i a n a . F .
culmorum. or CL gramineum.
In culture BL culmorum was
not sensitive to diclofop until exposed to 1,000 m g / 1 .
Growth
rate
of
CL
gramineum
and
sorokiniana
IL
reduced more by diclofop than that of
g r a m i n i s . Unlike
stimulation
due
the
other
to diclofop
c u l m o r u m or G.
f u n g i , jL gram i n i s
exposure
was
was
growth
noted at 10
mg/ 1 , despite a significant decrease in growth at I, 100,
and 1,000 mg/1. Since a foliar application could result
in
a 10 m g /1
stimulation
herbicide
in
jL
con tien,t ration
graminis
influence disease development.
uations
influence
indicate
Take-All
that
growth
at
in
10
the
soil,
m g /1
a
could
However, greenhouse eval­
diclofop
application
disease severity in wheat.
does
not
Further
tests under field conditions are needed to c onfirm this
observation.
Direct stimulatory or inhibitory effects of diclofop
43
on fungal pathogens were generally negative, although an
increase in wheat injury resulting from diclofop applica­
tion to infected
wheat
may be influenced by alterations
in host-pathogen relationships.
lished
to
evaluate
the
Field trials were estab­
combined
effects
infection and diclofop application.
testing
at two
locations
of
pathogen
Two yeaij-s of field
could not confirm
the observa­
tion that soil-borne disease infection decreases wheat
tolerance
to diclofop.
No increases in crop injury due to diclofop applica­
tion to wheat infected with F*. culmorum. B. sorokiniana.
G. graminis or (%_ gramineum were detected.
Conversely, a
reduction in disease effects on wheat yields was detected
where plants were inoculated with Bj. sorokiniana (P<0.1).
Positive
increase
disease-diclofop interactions resulted in an
in
yields
of
infected
wheat
treated
with
diclofop. IL_ sorokiniana interactions were significant
(P<0.1) at both Bozeman and Moccasin in 1982;
interactions were detected in 1983.
however,
no
Interactions with C.
gramineum and EL culmorum were not significant (P<0.1).
The positive B . sorokiniana diclofop interactions
may be related to soil moisture. Precipitation data are
recorded in Appendix A. Wet soil conditions could enhance
diclofop diffusion from the soil surface into the inocu-
Iation
zone
exposure
tial.
near
to the
the
seed.
herbicide
An
i n c r e a s e ' in
could
reduce
pathogen
inoculum
poten­
Results from toxicological studies have shown that
10 mg/1
diclofop inhibits grow t h of Bj. sorokiniana in
culture. Numerical calculations indicate that a broadcast
application of 1.12 kg ai/HA could result in a concentra­
tion of 10 mg/1 diclofop in the top 15 cm of soil.
Soil type may also influence pathogen exposure to
diclofop.
In heavy soils diclofop half-life is. 30 days,
while
in light
(Weed
Science
loam
soils
half-life
S o c i e t y , I 983) •
is reduced
The
silt
soils at Bozeman and Moccasin,
to 10 days
loam
and clay
respectively,
would
have a relatively slow rate of diclofop breakdown result­
ing in an extended pathogen exposure time. Interactions
may not be evident in lighter soils.
Additionally, the inhibitory effects of diclofop may
be more pronounced with art if ical inoculation. In this
situation the source of inoculum
is concentrated in a
single layer at the bottom of the furrow.
tends
to
collect
in
furrows,
soil
water
Since water
containing
diclofop would have a tendency to collect in the inoculum
zone.
Therefore,
be abnormally
tions.
pathogen exposure to the herbicide may
high
as compared to
natural field condi­
In a natural field situation inoculum y/ould be
45
more
unif o r m l y
distributed
throughout
the
root
zone.
Uniform inoculum distribution may decrease the likelihood
of pathogen exposure to the herbicide and may negate the
detrimental effects of diclofop on the pathogen.
No Fa_ culmorum interactions were detected.
evaluations
the
lack of detectable
In field
culmorum-diolofon
interactions could be due to high background levels of F.
culmorum.
levels
During
were
1982,
ne a r
30%.
in uninoculated
Su c h
infection could have obscured
non-diseased plants.
to diclofop
pathogen
could
a high
plots
percentage
interactions.
of
the effects of diclofop on
The higher tolerance of
also
infection
culmorum
account for lack of herbieidaIn
toxicological
testing
F.
c u l m o r u m showed no growth response on diclofop amended
media until exposed to concentrations of 100 mg/1.
Although C,^ s r a m i n e u m was sensitive to diclofop in
culture, lack of pathogen-diclofop field interactions may
be
related
to
time
of
infection.
Since
infection
of
winter wheat by C. c r a m i n e u m occurs in late February or
March, pathogenesis would be complete before herbicide
application in May.
on
JC4. g r a m i n e u m
disease
Therefore,
would
not
toxic effects of diclofop
be
effective
in
reducing
incidence.
Field
evaluations
of
Gaeumannomvces
graminis-
diclofop
interactions were unsatisfactory due to erratic
disease
development
wheat trials.
destroyed
in artifically
inoculated
spring
During 1982 severe G. graminis infection
artificially
inoculated
plots.
The
following
year no reliable field data with IL_ graminis was obtained
due to low levels of infection as well as crop damage
caused by hail. To overcome the difficulties associated
with establishment of inoculated field plots,
diclofon-G.
graminis interactions were evaluated Under greenhouse
conditions.
In normal pot culture, artifical inoculation did not
provide adequate disease development, therefore, a hydro­
ponic
system
was
developed
d i c l o f o n - G.grami n l s
diclofop
to
wheat
and
interactions.
infected
with
utilized
to
evaluate
The application of
graminis
did
not
increase levels of herbicide injury or disease injury.
In fact, herbicide response was less dramatic in roots
from (L. graminis infected wheat than in healthy wheat.
Therefore,
diclofop
despite
on
diclofop-induced
a direct
stimulatory
graminis
at
10
increases
in root
m g /I
in
damage
effect
of
culture,
no
were
observed
in infected roots compared to healthy roots.
Although hydroponic experiments indicated that there
were no herbicide-jIL. graminis interactions that could
47
account for increased wheat injury with diclofop applica­
tion,
further field evaluations are necessary to confirm
these
findings.
It is possible that d i c l o f op-induced
adventitious root pruning could decrease wheat tolerance
to Take-All disease.
increase
in wheat
fertilization
According to Garrett (1981),
the
tolerance to iL_ cram i n i s due to NPK
corresponds
to
increased
as a result of fertilizer application.
root
production
Prolific adventi­
tious root growth allows the plant to counteract the root
decay process induced by fL. eraminis.
reduce
the
adventitious root growth,
ability
of
graminis infection.
wheat
to
diclofop could decrease
escape
the
effects
of
G.
This mechanism could account for the
increase in Take-All disease
severity following diclofop
applications in Chili (R. Madariaga,
tion).
Since diclofop can
personal communica­
Field evaluations are necessary to measure the
importance of diclofop root growth inhibition on Take-All
disease severity under natural conditions.
Although
studies
with various phenoxy herbicides
have shown either direct stimulation or increased disease
incidence
with
Dreshslera
Madsen and Hodges,
and
Christensen,
Hunter,
1982);
1982);
1951;
sorokiniana
(Hodges,
1977;
Helminthosnorium sativum (Hsia
Richardson,
1957;
Fusarium spp. (Richardson,
Tinline
and
1959; Hissy and
I 98O); and Gaeumannomvces graminis (Nilsson,
Abdel-kader,
I 97 3 a b ;
Huber,
dicj-of op
were
Fusarium
1981);
no
observed
negative
with
interactions
Bi do Iar is
with
sorokiniana.
culmorum. Gaeumannomvces graminis var. tritici.
or Cephalosporium gramineum.
Since diclofop,
a diphenyl
ether herbicide, is chemically unrelated to herbicides in
the phenoxy class responses similar to those obtained
with
phenoxy
changes
pathogen;
no.t
herbicides
in root growth
interactions.
found
gramineum.
with
not
expected.
. However,
were suspected of altering hostSuch
negative
interactions
B_=_ s o r o k i n i a n a , F . c u l m o r u m
were
or
C.
Effects on G. graminis under field conditions
need further evaluation.
beet
were
research
in which
These results agree with sugarno interactions
between diclofop
and Rhizoctonia solani were found (Ruppel et al., 1 982.)
49
SUMMARY
Data from field and greenhouse studies indicate that
there is no increase, in expected levels of herbicide or
disease injury when diclofop is applied to wheat infected
with
JL_
s o r o k i n i a n a . F . c u l m o r u m r or
Cj. g r a m i n e u m .
Interactions between diclofop and soil-borne plant patho­
gens
were
p o s i t i v e , as
where yield
of infected
in the
wheat
case
of JL. sorokiniana
increased due to diclofop
applications,
In direct
induced
exposure
stimu l a t i o n
pathogen virulence
F. culmorum.
of
studies
there
was
no diclofop
mycelial gro w t h or changes
in
with JLu sorokiniana. C. gramineum. or
Conversely,
with IL_ graminis there was a
stimul a t i o n in grow t h by diclofop at 10 mg/1.
However,
data from greenhouse evaluations indicated that there
were
no increases in Take-All disease severity due to
diclofop application to infected wheat.
virulence
of
gram i n i s
were
noted
No changes in
after
diclofpp
exposure. .
Field data for diclof o p -G. graminis interactions is
incomplete.
sary
for
Improved
further
inoculation
evaluations
techniques
are
neces­
of jL. g r a m i n i s -diclofop
interactions under field conditions.
50
LITERATURE CITED
Altman, J. 1972. Increased glucose exudate and damping
off in sugarbeets in soils treated with herbicides.
Phytopathology 6 2:743.
Altman, J., and C.L. Campbell. 1 977» Effect of herbicides
on plant diseases. Ann. Rev. Phytopathology
15:361385.
B o l d t , P.F., and A.R. Putnam. I 980. Selectivity m e c h ­
anisms for foliar application of diclofop-methyl. I.
Retention, absorption, translocation and volatility.
Weed Sci. 28:474-477.
B o l d t , P.F., and A.R. Putnam. 1981. Selectivity m e c h ­
anisms for foliar applications of diclofop-methyl.
II. Metabolism.
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55
APPENDIX
Table 11. Growing season precipitation during 1982 and
1983 at Bozeman and Moccasin, Montana.
Precipitation (mm)
Bozeman
I 982
Month
Moccasin
1982
1 983
April
31.0
18.3
37.8
3.0
46.7
66.5
June
74.2
60.7
89.7
July
33.8
70.4
3.3
August
19.3
29.7
20.3
TOTAL
161 .3
225.8
217.6
- May
1D a t a from recording stations at the central Montana
Agricultural E xperiment Center, Moccasin, Montana and
the Arthur H. Post Agricultural Research Field L a b o r a ­
tory, Bozeman, Montana.
MONTANA STATE UNIVERSITY LIBRARIES
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