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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)]?