Our first meeting with the GENECO course will take place in the Ecology Building (Lund University) on Thursday, October 21 2010 (10.00 - 12.00). During this meeting, we will discuss chapter 1 (p. 3-17) and chapter 4 (p. 51-79). After this meeting, I expect the participants to be able to define and explain these terms:
- Homozygous effects
- Dominance coefficient
- Additive effect
- Average excess
- Breeding value
- Additive genetic variance
In particular, you should be able to explain how the link between breeding values and additive genetic variance, and how these terms are related to each other.
I also want you to discuss, in particular, the second paragraph on p. 17, about the relationship between molecular genetics and quantitative genetics. How do Lynch & Walsh counter the frequent criticism from molecular geneticists that quantitative genetics is "phenomenological", "missing the boat" or "cheating"? To what extent is it justified to ignore the details, studied by molecular geneticists, and focus on phenotypes? Do we actually need any information about mechanisms at all, to quantify and study patterns of resemblance between relatives? Would quantitative genetics work independent of the genetic material (i. e. whether it is DNA, RNA or any other self-replicating hereditary substance)? Why? Why not?
I recommend you to register your name at "Blogger" to participate in the discussion and comment on the posts below. Alternatively, you might sign with your name, but without being registered at Blogger. In any case, use this forum as a means to put forward your questions during the course.
First meeting, Linneaus University 2010-10-21
ReplyDeleteQuestions:
Regarding dominance, figure 4.7; why is the genotypic value decreasing with gene content 2 and dominance coefficient (k) higher than 1? What is a possible molecular mechanism behind it?
We had some difficulties defining and explaining average excess and to what use it is?
Good questions!
ReplyDelete1. The first one is due to the fact that dominance causes non-linearity in the genotype-phenotype map, and this is simply definitional (and independent of molecular mechanism). That is, with strong dominance (k > 1), the heterozygote is not intermediate between the two homozygotes, which is called "overdominance" when we talk about a character as fitness (you could put "fitness" on the Y-axis and replace "Genotypic value" to see this; then the heterozygote will be ABOVE the two homozygotes). Thus, this is more or less definitional and arises from how dominance is described and it need no molecular mechanism (i. e. it is independent of the mechanism Wright suggested).
Fig. 4.7c simply reflects this: with non-linearity in the genotype-phenotype map, the relationship between phenotype and genotype becomes "blurred" and moves away from linearity. It also means that allele frequencies change in the populations (note how the size of the dots change as you move from left to right), the SLOPE relating genotypic value to gene content also changes (due to these frequency changes). That is, this has to do with allele frequencies changing in the population, and there is no molecular mechanism involved (it is simply a population genetic process of shuffling around genetic variation, no evolutionary change in gene expression etc.). The effect arises as an automatic consequence of dominance, regardless of how dominance arises.
The second question, regarding the average excess, I will answer in a separate comment, but I need to think of how to formulate it in a pedagogic way.
One thing that we discussed, is the illustration of dominance in figure 4.6. Here it is shown that there are dominance effects also in the homozygotes (see also table 4.1). Maybe not very surprising, but this is something I haven't thought about before.
ReplyDeleteSecond meeting, Linnaeus University
ReplyDeleteWe have a question regarding Figure 17.2 on page 545.
Why is the optimum family size increasing when heritability is more than 0,6 in curve B and C?
I am not completely sure about this, but it might be due to the fact that in full-sib families (curve A, full-sib families), estimated heritability will always be somewhat higher since dominance variation also comes in to play. This means that it will be easier to reject the null hypothesis of no heritability, but not because it is a "better" method. Methods B and C have more potential information in them (half-sibs making it possible to estimate maternal effects, and mid-parent information), but to fully utilize the power of that information you might need larger sample size, I suppose.
ReplyDelete