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Biol258 Phenotypic Plasticity
Week 6- Chapter 5 of Pigliucci and Via et.al. Adaptive phenotypic plasticity: consensus
and controversy
Discussion Points
Pigliucci
QTL’s
(Ted 1) Why did the QTL’s (pg 111) become poor predictors of phenotype when
heritability was high, and vice versa? What is the significance of this?
(Amber 2) What does an LOD tell us, and how is it arrived at?
(Justin 1) It is suggested by Pigliucci that “previously unobserved patterns of
phenotypic plasticity can evolve quite rapidly” (pg 112). If this is the case, then what is
the rate of evolution, and how can it be measured? How would we expect the rate to
differ (i.e. between different traits, between genotypes)? What predictions can we make
with this knowledge?
What is a Plasticity Gene?
(Tara 2) Pigliucci’s definition of a plasticity gene seems vague, and he further
cautions against saying a gene is for something. How can we then define what is a
plasticity gene?
Molecular Genetics
(Tara 1) Since HSP70 (on pg. 118) can often be detrimental to an organism, and
further is not beneficial in responses to cutting and bruising, how then did it become
involved in these responses?
Epistasis and Pleiotropy
(Will 1) Will selection cause linkage of genes with epistatic interactions? Does
this happen in nature? Can’t selection prevent epistasis from constraining selection by
tying genes effecting phenotypes together? Is epistasis a long-term constraint of natural
selection?
(Amber 3) What is the difference between the quantitative genetics and
physiological definitions of epistatsis? How is this relevant?
Hormones
(Justin 2) Are there other aspects of organismal function (i.e. nervous
systems/neural nets) besides hormones that can be “at the interface between genes and
environment”?
Conclusion
(Jon 2) At the end of the chapter, Pigliucci separates molecular and evolutionary
biology into ‘how’ and ‘why’. He also seems to make the case that connections beyond a
level of ‘informing one another’ are not useful. Is this the case, and if so why devote a
chapter of the book to molecular biology?
(Ted 3) More a comment- Pigliucci, despite using a wide variety of experimental
data, often fails to describe the system studied (i.e. the organism and its’ relevant
features). This is even more surprising in a chapter where he is trying to unite molecular
and organismal biology.
Via et.al.
Reaction Norms and Models
(Greg 1) Why can’t we translate between the polynomial and character state
models when the environments are continuous? How is this different than the discrete
case?
Genetic Mechanisms
(Ted 2) Can we differentiate between allelic sensitivity and gene regulation
experimentally?
(Greg 2) Are ‘genes for plasticity’ only possible if the mean and plasticity of a
trait are independent? Can there be cases where the two are not independent, and a ‘gene
for plasticity’ exists?
(Amber 1) What role might temporal and spatial scale play in the debate over
whether reaction norms can directly be affected by selection? Might environmental
homogeneity lead to reaction norms that are by-products of selection on the mean
phenotype, while environmental heterogeneity lead to direct selection on a reaction
norm?
(Willow 2) How can we separate by-products of selection from intended products
of selection? Does selection work with intentionality? If not, isn’t everything then a byproduct?
Conclusion
(Jon 1) How effective is a ‘debate’ paper such as this one? Also, isn’t the
statement posed in the final paragraph merely the challenge of all experimental biology?
(Willow 1) If the shape of a reaction norm is determined by a groups’ response,
wouldn’t the idea of selection acting directly on a reaction norm shape be advocating
some form of group selection?
Actual DQ’s
Tara
1) pg 118-119. The section discussing common molecular machinery for a
multitude of responses to environmental conditions. I found it very
interesting that these organisms were producing HSP70 in response to
bruises and cutting. Although HSP70 can prevent damage to an organism
under high heat stress, HSP70 can be very detrimental to an organism
both while HSP70 is being produced and while there is residual HSP70 in
the organism. Since HSP70 is not beneficial for the repair of bruises
and cuttings, how do you suppose these two response became linked to
the same environmental or hormonal cues.
2) pg 113-116 Pigliucci spends a lot of time in this section defining
what a plasticity gene is and he finally sticks to the definition of
"regulatory loci that directly respond to a specific environmental
stimulus by triggering a specific series of morphogenic changes."
Lots of genes cause a wide variaty of responses to occur, whether
directly or indirectly. Therefore how are you able to make a
distinction of what is a plasticity gene and what is not?
At the end of the section he cautions you that a gene can't explicitly
be for something because you can never say for sure that the gene is
coding for any particular function. I know he is only trying to get
the point across not to think of any gene in absolute terms, but he
seems to be contradicting his whole argument. If you don't know what
the gene is coding for then how can you know if it is plastic or not?
Willow
1) On p. 216 of the TREE article (bottom of middle column), the authors
state that "In most cases, reaction norms probably evolve as by-products of selection on
phenotypic values expressed within environments, but selection may sometimes directly
change the form of a reaction norm." If selection is directly acting to change the shape
of a reaction norm, wouldn't this suggesting that there is group selection working, since
the shape of the reaction norm is usually determined by the response of group, rather
than an individual? Please help clear this up for me – I am feeling conflicted, since I
was always taught that biological dogma is that "group selection" is a dirty term.
2) In the TREE article (bottom, right column p. 215) the authors
describe a major conflict in thinking about phenotypic plasticity
between people who think that "the outcome of selection is determined
mainly by internal constraints that are reflected in genetic
covariances" and those who think that the evolution of plasticity
merely occurs as the by-product of "contingent occurences of novel
regulatory mechanisms and switch genes." If changes in the regulatory
mechanisms are the product of changes in the genes, and there certainly
are constraints on what material is available for selection to act
upon, then how can we separate a by-product from an intended product of
selection? Does selection work with intentionality, and, if not, isn’t
everything a by-product?
Ted
1) "If the trait had low heritability, the QTLs detected in the F2 turned out to be much
better predictors of the phenotype of the F3 offsprings than the phenotype of the F2
parent". I don't understand why this is an interesting by-product of the tomato study on
page 111 paragraph 3. Wouldn't it stand to reason that the F3 be closer to the F2 than
the F1? I guess the interesting part come in the next sentence: "If the heritability was
high, knowledge of the QTLs did not add anything in that respect". My next question then
becomes, why do QTLs of both F1 and F2 become poor predictors of F3 phenotype when
heritability is high?
2) In the Via et al. paper, they point out the two genetic effects that affect
plasticity: allelic sensitivity (Pigliucci def'n = modulation of phenotype through
development) and gene regulation (Pigliucci def'n = genes are on a switch...
developmental conversion). How can you experimentally differentiate between the two types
of genes for plasticity? Also, It would be very interesting if these types of plasticity
could be mapped to the two different types of environments (discrete and continuous). I
could see how gene regulation would be effective in discrete environments and allelic
sensitivity seems to fit with continuous environments.
3) One comment I have about this text, and it is suprising considering it tries to bring
together molecular and organismal disciplines, Pigliucci often does not describe the
organism or its relevant features when outlining case studies. On page 112, the genus
Populus is used without any description as to even which kindom it belongs. The genus
Populus are cottonwood trees. They belong to the willow/poplar family. They are large,
tall, deciduous, dioecious trees that reproduce either vegetatively or sexually. They are
the trees that produce those catkins with seeds that have white fluffy hairs. P.
trichocarpa is the black cottonwood and P. deltoids is the eastern or Carolina
cottonwood. They both live on low to medium elevation, in moist to wet sites
(floodplains, islands, disturbed upland sites). I can't tell the
difference between them except for bark color and slight leaf shape. From what I've read,
the black cottonwood is somewhat slightly more flood resistant. In the old days, the gum
from the buds was used in preparations for baldness, sore throats, whooping cough and
tuberculosis. I bet it tastes bad... but only if it grows in an area in which it may be
cut down and made into medicine.
Amber
1) In the paper, on page 216, first column, second paragraph:
"Considerable controversy has been generated about whether the shape of
a reaction norm can be directly affected by selection, or whether
reaction norms respond to selection only indirectly, through the
evolution of the mean phenotypes in each separate environment." Could
this controversy be somewhat resolved by considering the temporal and
spatial scale of the plasticity? Maybe, if an organism did experience
different environments over its lifetime, and was able to adjust to
these different environments, then perhaps selection could act on the
entire reaction norm/ plasticity gene. However, if the organism
experienced environmental homogeneity over its lifetime and never had
to express a different phenotype, then that reaction norm / plasticity
gene would never be exposed to selection and would only evolve as a
by-product of the selection on the mean phenotype of the population.
2) I must confess to having limited knowledge of QTL mapping, so I
would like to go through figure 5.1 on page 112 of the book.
Specifically, how is one of these graphs generated by a QTL study, and
what does LOD tell us?
3) Although I know that Marty went over this somewhat in his
introduction, I would like a repeat: What is the difference between
epistasis in a quantitative genetic sense and epistasis in a
physiological sense (page 123)? And what is Pigliucci's reason for
bringing up this distinction here, but not really linking it to any of
the studies that he's just finished writing about?
Greg
1) In the second column on page 213 Via et al discuss why it is not accurate to translate
between polynomial models and character state models when environments are continuous. I
don't fully grasp why this is the case, when they claim that you can translate between
the two models in the discrete case. The only difference I can think of between
continuous vs. discrete environments is that when you fit polynomials in the discrete
environment the ordering of the environmental variable will be arbitrary (e.g., how do
you order 3 different hostplants?).
2) I think I've brought up a similar subject before, but since I don't think the
proverbial horse is dead yet I'll bring it up again. Why would "the view that the mean
and plasticity of a trait are independent (lead) to discussions of possible roles for
'genes for plasticity'" (Via et al p 212, last column). Why wouldn't the view that trait
mean and plasticity are not independent lead to the same speculation? I can envision a
case where a regulatory gene that is induced in one environment and regulates plasticity
simultaneously mediates the trait mean. e.g., in Pigliucci's example of effects of
hypoxia on metabolism in Arabidopsis what if all genotypes performed equally well in
favorable conditions but there was large genetic variance for performance (e.g. ATP
production) under hypoxic conditions and
the shift to the hypoxic pathway is primarily due to genes only expressed under hypoxic
conditions? In this case wouldn't the regulatory genes (that are in effect 'plasticity
genes') influence both the trait mean and the plasticity (slope)?
Justin
1) On pages 111-112, P discusses a study of tomatoes that addressed
the ability of the plant to withstand salt stress. By crossing two
closely related species, the authors were able to identify 6 markers
affecting fruit number, fruit weight, etc. The study also uncovered a
marker that behaved oppositely of the expectation from parental means.
P states that "this suggests that the cross produced recombinants
with transgressive and therefore novel phenotypes, implying that
previously unobserved patterns of phenotypic plasticity can evolve
quite rapidly." What then is the rate of evolution of plasticity?
How would one measure this rate? This rate likely differs for
different plastic character traits, but does this rate differ for the
same trait among different genotypes? What predictions, e.g. re:
genotype-phenotype matching or organismal fitness, can be made by
knowing the rate of evolution of plasticity?
2) P devotes several pages in this chapter to the role of hormones in
plasticity research. Hormones may be principally relevant to plant
research, however P neglects to discuss neural modes of control in
animals. For example, the human autonomic nervous system is divided
into sympathetic and parasympathetic halves that are responsible for
quite distinct forms of neural control...e.g. regulating organ
function to stimulating hormone secretion from glands. Lower animals
likely do not possess neural nets that are as highly structured, but I
imagine that they are equally as important as hormones in regulating
plastic responses to environmental variability, albeit on a different
temporal scale. In light of this issue, what other aspects of
organismal function may be considered "at the interface between genes
and environment?"
Jon
1)Via et al. This is an interesting approach to resolving conflict: write
a paper together! I'm wondering how effective it is since each statement
is followed by a "however' from one of the other authors. I kept getting
confused about whether the character state method really was better in
certain siutuations than the polynomial model. That's not really a
question, more of a statement. Another question is regarding the last
paragraph. Isn;t this the challenge for experimental biology in general?
2) As usual Pigliucci got me bogged down in the specific examples and I
lost the main message of his chapter (to some extent). If molecular
biology and evolutionary biology are so distinct (how vs. why) then why
include a chapter on them? I feel like he wanted to make an argument for
the use of molecular biology in questions about the evolution of
plasticity but then he took the wind out of his sails at the end by making
those statements. Why would he do this? Is it to appease the evolutionary
biologists who cringe at molecular methods? Or does he really feel it's
unneccessary to make connections between the two at more than the 'they
inform one another' level?
Will
Pig brings up (p. 115) the argument that you must be careful arguing that
"genes for" something exist because of the exaptation/adaptation argument
and because of pleitropy and epistasis. If made me think about how
selection should act on genes with epistatic effects. This question may seem off the
wall and unrelated to plasticity, but:
1) Would you predict that selection on phenotypes would cause linkage between genes that
have epistatic interactions such that coadapted alleles would be linked together?
2) Does this happen in nature? I seem to remember this type of correlation from genetics
10 years ago, but somebody help me out here.
3) Aren't hormone-controlled gene pathways an example of selection tying
"genes for" particular phenotypes together and preventing epistatic
effects from constraining selection?
4) If selection acts for a long enough time, won't the alleles that work
best together become most abundant in the population so that epistasis is
not a long-term constraint on natural selection?
5) Would it be better to view epistasis as the result of relaxed or
disruptive selection on a phenotype than as a true constraint? What about
plasticity [maybe I am making via's argument (p.113)]?