3000-'13-3d
Oct 15
Exam and grades
• Why is percentile more
useful than percentage?
• How to interpret your %ile:
about 33-35 is the C/B line
• Depends in part on
distribution, how wide
variance
2012
grade
%
%ile
A
86+
90+
A-
82+
78+
B+
76+
61+
B
72+
45+
B-
67+
34+
C+
64+
23+
C
54+
10+
C-
51+
7+
D
43+
2+
is the wiki helping you?
• has evolved into a
resource for alternate
explanations
• many interesting
studies posted there,
hasn’t quite taken on
life of its own...
might i suggest...
• don’t be passive
learners. alternate
explanations good;
explaining it to
yourself and others
is better.
• get into arguments!
edit over each
others stuff to make
it better!
antibiotic resistance
• can it be reversed?
less than half the time
• when no antibiotic present,
wild-type (sensitive)
bacteria have higher fitness
but still often lost to drift
• resistant bacteria have
multiple “compensatory”
pathways for minimizing
fitness difference
w11=1, w12=0.95,
w22=0.9
so the antibiotic resistant/susceptible work fits with
what we have learned before about drift vs. selection,
among other things!
where we are going
• we have today and 3 more lectures
before exam 3 on 10/29
• adaptation (chapter 10) and sex
(chapter 11) are my goals
• read. do problems at end of chapter.
come to class. go to discussion
(remember this is 4 credit hours).
contribute thoughtfully to wiki.
adaptation
• now we are talking about the evolution of complex
traits - not just quantitative, but multi-factor, different
parts working together (“complex adaptation”)
• sometimes new gene functions (following gene
duplication, for example), sometimes co-opting
existing functions
• interaction of multiple genes and gene regulatory
networks
evolution in the lab
• Lenski experiment with
multiple lines of E. coli
growing in lab for 20 years
evolution in the lab
• Lenski experiment with
multiple lines of E. coli
growing in lab for 24 years
• that is 55000 generations!
• 2008: 31,000 generations
in, one flask grew faster
*a
defining
feature
of
because it was using citrate
E.
coli
:
they
can’t
eat
for food
citrate!
evolution in the lab
• actually E. coli can eat citrate, but only in O2-free
environments: switches on citT gene, helps
exchange one compound for citrate
• around generation 31,500 one bacterium
accidentally duplicated citT, new copy near a
switch that is “on” in presence of O2
• eventually duplication of THIS arrangement
improved metabolic ability
evolution in the lab
• here’s the cool part: go back into the freezer prior to
generation 31,500
• bacterial stocks AFTER generation 20,000 restarted in longterm experiment; some of them evolved citrate metabolism
• prior to 20,000: nada
• if they supply post-20k stocks with a plasmid that carries
citT+O2 switch, it can eat citrate. pre-20k stocks: nada
• another mutation was required that ALLOWED the second
mutation to work!
• “
It’s remarkable how this experiment contains many
elements of
evolution that scientists have noted in other species. It’s
genes to get duplicated, and for
the new copy to be rewired for a new
job. Snake venom, to pick one example, also evolved
common for
when genes were accidentally copied and then rewired.
A gene that originally produced a digestive enzyme in
the pancreas, for instance, now started making that
enzyme in a snake’s mouth. It turned out to be a crude but effective
venom. Later mutations fine-tuned the new venom gene until it became wickedly
good.
•
The only important difference is that it took millions of years for snakes to evolve
their arsenal of venoms, and scientists can only reconstruct their evolution by
comparing living species. But in the case of E. coli, the transition unfolded fast
enough for someone to track it from start to finish–and restart it when
necessary.
”
• -Carl Zimmer (one of the text authors)
general case: gene
duplication
paralog:
distinct gene regions of
homologous origin
in same genome
paralogy in snake
venom
identifying gene
duplication
true phylogeny
sequence genes
species A
outgroup
species A
outgroup
species B
species C
duplication!
species A
outgroup
species B
species C
species B
species C
species B
species C
“pre-adaptations”: some changes
seem small but needed for the “big”
changes to happen
many changes
leading to evolution
of venom
gene regulation
• duplication and mutation are one mechanism;
changing how, when, where a gene turns on is
probably more important
• language: cis is Latin for “same side of”; trans is
Latin for “across from”
• cis-regulatory regions are stretches of DNA near
to/attached to the gene in question; trans-regulation
involves a product from elsewhere in genome
so is cis or trans
affecting regulation of
generegions
X? both.
• cis-regulatory
are the portion of
genome attached to a gene that
INTERACT with environment (small
scale!) to determine on/off status of
gene
• the environment is defined by transregulatory elements: gradients of
proteins and other products in tissue of
organism
even-skipped gene
segmentally-expressed
genes important
for modular development
of many organisms
3 hypotheses for
segmentation
understanding
phylogeny helps us
understand our own
development!
3 gains
2 gains, 2+ losses
1 gain, 3+ losses
Metazoans phylogeny
work in progress
MANY More genes
how it works: cis regions turn on
given gradient in trans agents
patterning from external
environment to embryo
diffusion
gradient
of trans-reg
factor
copies of gene
and regulatory region in
cells along axis of body
evolution of
development
• the role of regulatory elements in development
of traits, body plans
• may be subtle: new metabolic pathways used
• may be profound: entirely distinct body plan
• “evo devo”