Biol 258--week 2
Full DQs
Amber1: My first question concerns the discussion of heritability and Figure 1.2e on page 9. Figure 1.2e is the
reaction norm graph that shows 2 reaction norms, both with positive slopes not equal to zero, and not parallel. Thus,
this illustrates a situation in which there is genetic variation, plasticity, and variation in plasticity. On page 9,
Pigliucci points out that in this figure, on the left part of the environmental gradient, the reaction norms nearly
converge, indicating an estimated heritability of zero. In contrast, on the right part of the environmental gradient, the
reaction norms are quite different and the trait probably has high heritability. Thus, he points out that in the first
environment, selection on this trait would be ineffective, but in the other environment, it would work well. Could
this perhaps have implications for speciation? I was imagining a population (living in environment 1) in which a
group might have dispersed to a different environment. This group might then be exposed to selection acting on a
trait that previously had close to zero heritability. Could this possibly lead to divergence? If the trait that was
exposed to selection was, say, a trait for reproductive structures, I would think this new population might soon
become reproductively isolated from the source population.
Amber2: this isn't exactly a question, but I had difficulties with the last section of the chapter, "Environmental
Effects on the Multivariate Phenotype: Plasticity of Correlations and Correlations of Plasticities." No matter how
many times I read the definitions of phenotypic integration and plasticity integration, I just couldn't get the meanings
through my head. Also, I had problems with interpretation of the figures on pages 26 and 27. I know that I would
benefit from a summary and clarification of this section.
Amy1: Pigliucci makes the case (sort of) for heritablitiy to potentially increase, decrease, or remain unchanged in
unfavorable (stessful) environments (pg 11). His justification for potential INCREASE is that "1. Stress alters rates
of mutation or recombination. 2. Selection seldom occurs in novel or rare (and presumable stessful)
environments...." On a simply intuitive basis, I disagree with the second statement. Wouldn't stessful environments
be where selection most often takes place with the novelty and rarity determining the spread of selection?
Amy2: What does P mean by "plasticity for fitness" (pg 23)? He states it is maladaptive (that makes sense), but in
the Via example he used he states that that is what she found.
Greg1: So I understand why, as defined on pages 6 and 7, the mean genotype and the plasticity are mathematically
independent, but I'm having a little trouble visualizing genetic mechanisms that would cause them to be interrelated.
Are there any specific examples of this, empirical or theoretical?
Jennifer1: The traditional hypotheses for genotype-phenotype mapping function were broadened to incorporate
environment and epigenetics. Are there any other components that influence plasticity that could be incorporated
into the function?
Jennifer2: Phenotypic plasiticity is a response of the genotype to distinct environmental conditions. What exactly
constitutes a "distinct" environmental condition? Ex. is a change in temperature of a couple degrees enough to make
the environment significantly different, and thus influence plasiticity? In other words, what would be the minimal
requirements for plasticity to occur?
Jon1: Definitions of phenotypic plasticity confuse me. They confuse me because they seem to be so inclusive. I
suppose some traits are not plastic under Pigliucci's definition (e.g. eye color) but many traits are (e.g. weight or
height) that for some reason don't jive with my naive concept of plasticity. An example is weight, in an environment
with lots of food many animals get big and fat, in an environment without food they're smaller and skinnier. For
some reason I usually think of plasticity as being something more than this, maybe because examples in the
literature often deal with more striking phenotypic differences? I guess my question here is, should definitions of
plasticity be restricted to exclude general cases such as my weight gain example? Or, is plasticity interesting because
it's such a widespread phenomenon (under pigliucci's definition)?
Jon2: A question about figure 1.4 and the discussion of it on pg. 18-19. Why is there no genetic variation detected in
the ANOVA results for the third row? There is clearly genetic variation across environments (left hand side) and this
is identical to (but opposite in sign to) the top row. The text explanation is that the means across environments are
the same and therefore the ANOVA will not detect the variation. Is the purpose of this example to show how
particular analyses can be misleading without biological interpretation? I got bogged down in figuring out how there
was no genetic variation and now I can't seem to figure out the point of it.
Justin1: In the first full paragraph on page 8 of the text, the author describes the difference between the degree (or
amount) of plasticity, and the pattern of plasticity. The pattern of plasticity being the fact that all reaction norms in
Fig. 1.2 depict increasing trait values with increasing environmental values. On the other hand, the slope of the
different reaction norms varies; this slope "directly quantifies the degree of plasticity. My question is: In a
population, is it possible to quantify how much variation in the degree of plasticity must exist (or is necessary) in
order for selection to act upon plasticity as a trait?
Justin2: In the first full paragraph on page 12 of the text, the author describes a study by Jain (1978) in which this
author measured plasticity of flowering time in parents and offspring and then performed a parent-regression
analysis to determine the heritability of plasticity. The results showed that the population with the higher genetic
variance for flowering time also had the highest heritability for the plasticity of flowering time. Is this situation
likely to be found often, where populations with high genetic variance for a trait are also likely to be highly plastic
for that trait?
Marty1: What effect do regulatory genes and processes have on the study of phenotypic plasticity? Regulatory
genes themselves may exhibit some sort of plasticity, yet their effects can do away with phenotypic plasticity. An
example of this might be body temperature in endotherms- a variation in environment produces little( if any) change
in body temperature, yet regulatory processes alter radically to ensure the stable body temperature. Should special
consideration be given to regulatory processes when studying phenotypic plasticity?
Marty2: Are there potential connections between studies of speciation and phenotypic plasticity? Though not
mentioned in the readings, it seems possible that plastic phenotypes (especially if the associated genotypes were to
show preferential mating) might lead to a separation of populations. Imagine for example a situation where this
might be a plot of the phenotype
| /
| / genotype A
| /
|/
|/
|\
|\
| \ genotype B
| \
|__\______________________________
I
II (environments)
If environment II were present for long periods of time, and there were incomplete dominance, such that genotype
AB was less fit than either genotype AA or genotype BB, then it might be the case that two separate genotypes
would form initially separate subpopulations and then entirely separate species. Is this a valid avenue of exploration
in the study of phenotypic plasticity?
Marty3: I found the section of the chapter dealing with Bennington and McGraw's experiment through the Hoffman
and Merila section on heredity to be confusing and thought discussion might be useful. Much of it seemed obvious,
and I don't understand the importance Pigliucci attributed to the Bennington/McGraw paper, and sections of the
Hoffman/Merila paper seemed downright wrong to me (a comment along the lines of-no selection will occure in a
novel environment, allowing an increase in Vg). I'm curious as to whether on not I'd missed a deeper point in this
section, whether I'm looking at this wrong, whether it's supposed to be obvious or not, or something else.
Tara1: from page 8- There is no accepted method for quantifying the degree and pattern of phenotypic plasticity for
more then two environments. But in two environments researchers do not preform regression analysis. The two
points are simply connected graphically and either the angle or the difference is measured. Why can't this be done
for more then two environments. Obviously you could not look at the angle created, but if all you are looking at is
the difference between the two why can't you use bar graphs and compare the differences that way between multiple
environments?
Tara2: form page 14- Problems related to visualization of phenotypic plasticity as a property of a reaction norm.
When you mix different factors environments are plotted arbitrarily, so you can't have a continuous norm. Why do
you then assume the discontinuous reaction norms are sampled at one extreme of a gradient? If you are dealing with
multiple factors why can't they be plotted separately? This way wouldn't there be continuous reaction norms for each
trait,which would then reflect trends not extremes for each trait?
Ted1: I remember you trying to explain the phenotype vs. environment graphs during the last class, and I thought I
understood it. I was trying to work through the graphs in 1.4 and found that I was getting confused between the
terms "genetic variation for plasticity", "plasticity", "character mean" and "genotypic mean". Independantly, they all
mean something to me as defined in the paper, however I'm confused as to how they are represented in the all
important phenotype vs environment graphs.
Ted2: Also, the genotype phenotype mapping function, as I understand it, is a conceptual algorithm that includes
several variables, such as epistasis (the suppression of a gene by the effect of an unrelated gene), pleiotropy (when a
gene determines more than one unrelated characteristic), and epigenetic factors (non genetic phenotype
modifications). There are examples of heritability and evolution of plasticity, which suggests that plasticity can be a
phenotypic character itself, which sounds very complicated in itself. So I was wondering, can those other variables
in the G -> P mapping function also be heritable and phenotypic characters?
Will1: Is it really possible to elucidate the model of the genotype-phenotype matching function? If you determine
the function for one organism, how will it be related to the function in other organisms?
Will2: Phenotypic plasticity is a huge problem for systematists and conservation biologists because it influences
population differences and can only be controlled for by genetic analysis of population differences. Can research on
phenotypic plasticity be useful in predicting what types of population differences were likely to result from plastic
responses and what differences are most likely genetic?
Will3: On page 26, Palugiazzio states that studies of plasticity integration will play an important role in modern
evolutionary biology. Can we come up with hypothetical or real species groups where the correlation of plasticity of
different characters would have important evolutionary effects?
Willow1: Using a specific organism as an example, what is the difference between plasticity, reaction norm, and
character mean?
Willow2: Given the difficulty of ranking an environment from a species point of view (page 15, top of paragraph),
what are the practical applications of modeling phenotypic plasticity in this manner?