Epigenetic Factors as 'Creative' influence in Evolution

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It seems to suggest that genetic mutation does not play that much of a role in developing new variation but rather changes in development of the organism

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That would be a bit extreme as much of epigenetic regulation like DNA methylation and histone acetylation are themselves under genetic control and the genes responsible, under selection. Also, epigenetic states are heritable i.e. you express specific maternal or paternal alleles of imprinted genes. There are several hypotheses for the evolution of imprinting including maternal versus paternal conflict.Here is a really good review article on the subjectNat Rev Genet. 2003 May;4(5):359-68. Related Articles, Links
What good is genomic imprinting: the function of parent-specific gene expression.Wilkins JF, Haig D.Society of Fellows, 7 Divinity Avenue, Harvard University, Cambridge, Massachusetts 02138, USA. jwilkins@cgr.harvard.eduParent-specific gene expression (genomic imprinting) is an evolutionary puzzle because it forgoes an important advantage of diploidy--protection against the effects of deleterious recessive mutations. Three hypotheses claim to have found a countervailing selective advantage of parent-specific expression. Imprinting is proposed to have evolved because it enhances evolvability in a changing environment, protects females against the ravages of invasive trophoblast, or because natural selection acts differently on genes of maternal and paternal origin in interactions among kin. The last hypothesis has received the most extensive theoretical development and seems the best supported by the properties of known imprinted genes. However, the hypothesis is yet to provide a compelling explanation for many examples of imprinting.In any case, you don't need epigenetics to have an effect on development. The environment can alter development in many ways regardless of genetic background i.e. phenocopies or thalidomide for that matter.Where epigenetics, genetics, and development overlap is a new discpline called evolutionary development which takes into account that genetic variation is only part of the the story of morphological variation as development and environment also have an enormous impact on the final outcome of embryogenesis.

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The other end of the scale is less researched. Clearly the environment can exact a change on an organism that is not coded at all in its genome but whether the environment can trigger an adaptive reaction that can be selected for with out genes coding for most of the behavior is what I believe is open to debate.

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Certain heritable phenomenons that have nothing to do with genes have been produced in fairly simple organisms.

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Hi PR, I think I am losing the intent of the thread but it is probably my fault. As a molecular biologist, when you say epigenetics it means heritable and mutable DNA methylation patterns, histone acetylation etc. These are subject to mutation like DNA but if you sequenced both an unmethylated and methylated allele of a gene, you would get the same sequence and thus it is "epi"-genetic. That development can be affected in non-heritable ways is clear. If something causes gene expression of a hox gene to be delayed or increase or decrease, this will have an effect on the overall expression gradient of the hox gene which in turn will have an effect on all the genes in expression gradients with which it interacts. So a small change can have an amplified effect. However, this will not be a heritable change. You can however, inherit a methylation pattern from your parents and thus have paternal or maternally imprinted genes like the H19 gene or Igf2r. With development, the genes set out a potential blueprint for development but environment will play almost as much of a role in getting from the gene to the individual...that is why if you cloned a human, the clone may very well not resemble the original behaviorally and would likely be morphologically different.

Hi PR,
I think most of the examples you provide are genetically based. For example, if an environmental cue causes a transcriptional response in an adult (particularly the germline) and this alters chromsome methylation, histone positioning, etc. in a heritable manner, then it is a change in an epigenetic mechanism with a molecular basis (though the DNA sequence remains unchanged). Another important feature of development has to do with maternal effects. Female eggs contain a lot of RNA's, trancription factors etc. that are critical to development once fertilization takes place. Eggs sit around in the female carrying them for a relatively long time before fertilization takes place and are thus influenced by the environment. This may be why for example, Downs syndrome is more common if the mother is over 40.In all genetic experiments looking for "pro-active" or "pre-adaptive" mutation, the conclusion has been that it does not occur. Epigenetic modification is a more recent discovery but still operates under the principle of heritable change and selection on that change i.e. if you mess up parental imprinting, it either leads to miscarriage or disease like Prader-Willi Syndrome.

Here is another reference studying rates of adaptation and the effects of the environment on the rate of adaptation..note, it is genetic in originGenetics. 2002 Oct;162(2):557-66. Related Articles, LinksFitness evolution and the rise of mutator alleles in experimental Escherichia coli populations.Shaver AC, Dombrowski PG, Sweeney JY, Treis T, Zappala RM, Sniegowski PD.Department of Biology, University of Pennsylvania, Philadelphia 19104, USA.We studied the evolution of high mutation rates and the evolution of fitness in three experimental populations of Escherichia coli adapting to a glucose-limited environment. We identified the mutations responsible for the high mutation rates and show that their rate of substitution in all three populations was too rapid to be accounted for simply by genetic drift. In two of the populations, large gains in fitness relative to the ancestor occurred as the mutator alleles rose to fixation, strongly supporting the conclusion that mutator alleles fixed by hitchhiking with beneficial mutations at other loci. In one population, no significant gain in fitness relative to the ancestor occurred in the population as a whole while the mutator allele rose to fixation, but a substantial and significant gain in fitness occurred in the mutator subpopulation as the mutator neared fixation. The spread of the mutator allele from rarity to fixation took >1000 generations in each population. We show that simultaneous adaptive gains in both the mutator and wild-type subpopulations (clonal interference) retarded the mutator fixation in at least one of the populations. We found little evidence that the evolution of high mutation rates accelerated adaptation in these populations.

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Cognition processes are caused by a mixture between genetic and environmental factors? I think the part of genetics is only important in regard to brain development.

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It actually goes beyond brain development. Mice with mutations in the mono amine oxidase gene (MAO) are highly aggressive. There are similar psychiatric disorders in humans associated with this gene regardless of environment i.e. predominantly genetic effect. In addition, small genetically determined changes in gene expression, particularly developmental genes, can have wide repercussions for cognition. Downs syndrome is genetic and has a clear effect on later cognition regardless of environment. However, once the brain is formed, most cognitive determinants will be environmental as you state. But genetics and epigenetics can have a profound effect as well throughout life.