Epigenetic studies are burgeoning; these genetic mechanisms that are external to direct DNA/RNA encoding and expression are being intensively studied, particularly how environmental factors can stimulate methylation and acetylation of bases of DNA or histone proteins, and how this affects expression or repression of specific gene activity.
In particular, behavioral epigenetics studies the brain for epigenetic changes following exposure to specific behavior. The old Biblical idea of the father’s sins being visited on the son, or the ideas of the heavy influence of childhood experience on subsequent adult behavior now have some possible molecular genetical explanations via an epigenetic mechanism. Some of your grandma’s experiences might produce methylation/acetylation of the DNA of specific cell types, in specific regions of the brain, and might persist in grandma, producing a specific and repeated behavior in grandma, and this repeated behavior then effects the behavior of her children, such behavior producing methylation or acetylation of the DNA of specific cell types, and might persist in grandma’s offspring, producing a specific and repeated behavior in grandma’s offspring, and this repeated behavior then effects the behavior of their children, and so on.
This has been described as a possible mechanism for the nurture side of behavioral influence, something quite new in molecular genetics, which prior to epigenetic studies only provided support for the nature part of the argument (you inherit your DNA, with its code for biological specificity, from your ancestors).
However, suggestions that ‘grandma’s experiences leave epigenetic marks on your genes’ would seem to overstate the case. The verb leave proves to be a critically poor choice, as it suggests that from grandma, through the intermediary of one of your parents, you received DNA that was already specifically methylated / acetylated via her experiences. There is as yet no direct connection between the methylation/acetylation of DNA in somatic cells, and the transmission of these specific methylation/acetylation modifications to the germ cells (sperm or egg) of the organism in question, something that would have to happen if grandma were to leave them for you.
How would such DNA modification be inherited through ordinary germ cell DNA replication? Lamarck postulated that behavior could modify an organism in such a way that the new behavior could be passed on to subsequent generations. Biological science has found no support for this argument in the past, and much support for natural selection of existing genes in the gene pool, with gene variation coming from various mechanisms.
The nascent field of epigenetics provides some support for Lamarckism, that there appears to be some mechanism for passing on certain environmentally influenced genetic changes, but their is no evidence that this mechanism operates through germ cell replication of DNA, and in fact it would appear that without the same specific environmental trigger, the epigenetic modifications disappear, and with it, any future inheritance. This idea is controversial, and as yet there is only tantalizing hints that such a thing might be true. Some evidence points away from such a conclusion: As part of meiosis, the process of generating new germ cells in eukaryotic organisms, chromatin (DNA and their histone backbone) is entirely wiped clean of the methyl and acetyl groups added by epigenetic modification.
Complicating this idea is that the current model of genetic expression could just as well explain these phenomena. Epigenetic methylation/acetylation attaches acetal or methyl groups to DNA or histone proteins to either turn on expression of a gene or turn it off, and thus is part of DNA-driven regulation of genetic expression. This methylation/acetylation is controlled by enzymes, which themselves are coded for in an organism’s DNA.
lac operon. Top: The gene is turned off. There is no lactose to inhibit the repressor, so the repressor binds to the operator, which obstructs the RNA polymerase from binding to the promoter and making lactase. Bottom: The gene is turned on. Lactose is inhibiting the repressor, allowing the RNA polymerase to bind with the promoter, and express the genes, which synthesize lactase. Eventually, the lactase will digest all of the lactose, until there is none to bind to the repressor. The repressor will then bind to the operator, stopping the manufacture of lactase.. Attrib: T A RAJU, CC-BY-SA-4.0.
It has been clear since the Monod-Jacob lac operon model of genetic regulation was demonstrated in the early 1960’s that environmental influences are often a part of the control of genetic expression. In the case of the lac operon, the presence of lactose sugar in the environment of E. coli bacteria stimulates the construction of the enzyme lactase, which catalyzes the breakdown of the lactose sugar, a disaccharide, into two mono-saccharides. The presence of high titres of lactose unblocks the gene, the DNA sequence for lactase, allowing it to be transcribed into mRNA, and subsequently to be translated into the protein lactase by tRNAs and rRNAs. It may well be that methylation/acetylation of DNA or histones are mediated by similar environmental influences which at root are the final mode of control exhibited by regulatory enzymes, in a manner analogous of the lac operon.
This is a fascinating model for the control of gene expression, extending and complementing genetic control mechanisms like the lac operon. But the early suggestions of epigenetic inheritance, significantly different in character than Darwinian inheritance, is much more problematic, with some evidence pointing to epigenetic modification persisting across generations, but most pointing away from that. There is much debate in the genetic community about the possibility of epigenetic inheritance, and the consensus appears to be that it is not proven at this point. But all agree that the issue is not settled: Lamarck may be stirring, but has not yet been revived.