But nothing in the heat stress protein had anything to do with epigenetic DNA methylation.
I guess when all you have is a hammer problems look like nails.
==But nothing in the heat stress protein had anything to do with epigenetic DNA methylation
Are you sure? I don’t know much about the subject, but I found paper after paper studying how epigenetics relates to your heat shock proteins. Here’s just one example:
“Epigenetic and classical activation of Entamoeba histolytica heat shock protein 100 (EHsp1”
http://www.epidna.com/showabstract.php?pmid=16263115
Here’s another reference to the connection to heat shock and epigenetics from the link I sent you above. You know the link...it’s the one that prompted you to say “But nothing in the heat stress protein had anything to do with epigenetic DNA methylation...I guess when all you have is a hammer problems look like nails.”
Does the following mean that your third example has also bit the dust?
From the article:
According to Vercelli, the environmental susceptibility of epigenetics probably explains why genetically identical organisms such as twins can have dramatically different phenotypes in different environments. She points to the agouti mice, as well as another recent cluster of studies on a heat shock protein, Hsp90, in Drosophila melanogaster, as “model systems that have very eloquently demonstrated” the critically important role that epigenetic inheritance plays in this kind of gene-by-environment interaction.
Hsp90 regulates developmental genes during times of stress by releasing previously hidden or buffered phenotypic variation. Douglas Ruden of the University of Alabama, Tuscaloosa, says he noticed some weird fruit fly phenotypes—things like appendage-like organs sticking out of their eyes—at about the same time that a paper appeared in Nature connecting Hsp90 activity in Drosophila to genetic variation.8 In that paper, Suzanne Rutherford and Susan Lindquist, then at the University of Chicago, presented compelling evidence that Hsp90 serves as an “evolutionary capacitor,” a genetic factor that regulates phenotypic expression by unleashing “hidden” variation in stressful conditions.8 Even after restoring normal Hsp90 activity, the new phenotypes responded to ten or more generations of selection. The scientists concluded that, once released, even after normal Hsp90 activity was restored, the previously buffered variation persisted in a heritable manner, generation after generation.
https://notes.utk.edu/bio/greenberg.nsf/0/b360905554fdb7d985256ec5006a7755?OpenDocument