First, how can epigenetic traits be passed on to subsequent offspring, as seen with changes in mouse hair color, when epigenetic changes don't effect the DNA sequence of the organism? Does it have to do with some retaining trait of the chromosomes during meiosis?
The answer is probably yes, depending on what you consider to be a 'trait of the chromosomes'. In the case of the mouse agouti example it is a question of methylation state of cytosine residues in a transposable element (IAP) which is upstream of the
Agouti gene and creates the
Agouti Viable yellow allele.
So while the phenotpyic variation associated with the
Agouti Viable yellow allele is the result of epigenetic changes the allele itself is a traditional DNA based variant.
The methylation state of the IAP element is the basis of the variation, when the IAPs cytosine residues are highly methylated it its transcription driving activity is silenced, when unmethylated and active it serves to drive ectopic expression of the
Agouti gene, this is called the pseudoagouti phenotype.
When pregnant
Agouti Viable yellow mothers are fed methyl donors in their diet their offspring will tend towards a higher proportion of pseudoagouti phenotypes, this occurs over a large span of development, it is not neccessary to target the zygote and it certainly isn't a case of an effect from the gamete's, although the
next generations gametes will be affected by their
in utero exposure (
Cropley et al., 2006;
Cropley et al., 2010)
I also heard that most of the epigenetic information in sexual species is contained in the mother's DNA (so in the egg gamete?), is that why changes in diet while pregnant can change the offspring physically?
There are a couple of things here, one is that the difference in epigenetic marks between maternal and paternal genome complements is part of another phenomenon called imprinting which is somewhat distinct from what is happening with the
Agouti Viable yellow mice. The other is that dietary changes can readily affect phenotype without any sort of epigenetic mechanism, i.e. a lack of folic acid can lead to spina bifida.
Next, why is it thought that epigenetic changes have a more profound impact on micro-organisms, particularly single celled organisms, than multi-cellular life?
The main reason is that when a bacterial cell replicates then the epigenetic state of the daughter cells is much more closely linked than in the case of a multicellular organism which will have a wide variety of epigenetic states amongst the cells making up the organism. So epigenetic state inheritance in bacteria is much more direct. In many ways the equivalent thing to look at would be the epigenetic changes between different cell lineages within a developing multicellular organism rather than between multicellular parent and offspring organisms.
This means that in evolutionary terms epigenetic inheritance is liable to play a much greater role in bacterial than multicellular populations.
In terms of multicellular/metazoan populations it isn't clear yet what if any role epignetic inheritance such as in the
Agouti Viable yellow case is, the effects are very transient so there is no stable inheritance, but the existence of that allele at all gives rise to a wider spectrum of colour variation in a population that is genetically identical, which might have evolutionary consequences.
Imprinting has much better claim for an important role in evolution, particularly in the interactions between male and female parents. One of the major factors in imprinting is what is called parental conflict, where fathers want their offspring to gain as much of the mothers resources/nutrients as possible while mothers want to limit their expenditure to increase their future breeding potential (
Moore and Reik, 1996). So at least in mammals imprinting forms an important part of an arms race between the sexes.
I very much doubt any of these things have anything to do with punk eek.
TTFN,
WK
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