Ruefully, true scientists admit that every answer asks a thousand new questions. “Let's map the human genome?” they said, assuming that genes explain everything and that there are a hundred thousand of them. And they did. The map part. But then it turns out that only about a third of that many are code for making protein and the rest were -- um, “junk.” (The map is not the territory.) But then it turned out that they WERE code, but code for turning the other genes on and off, genes for timing, coordination, and so on. One third of the genes were the keys of the piano -- the others were the sheet music. The result was the creature, which was a symphony. And which has a personal style because every individual "plays" its chromosomes differently.
Here’s the high tech Wiki, presumably written by Someone Who Knows, so I left the links:
DNA methylation is a biochemical process whereby a methyl group is added to the cytosine or adenine DNA nucleotides. DNA methylation stably alters the expression of genes in cells when cells divide and differentiate from embryonic stem cells into specific tissues. The resulting change is normally permanent and unidirectional, preventing a cell from reverting to a stem cell or becoming a different cell type. DNA methylation is typically removed during zygote formation and re-established through successive cell divisions during development. Some methylation modifications that regulate gene expression are heritable and cause genomic imprinting, and hydroxylation of methyl groups occurs rather than complete removal of methyl groups in zygote.[1][2]
DNA methylation suppresses the expression of endogenous retroviral genes and other harmful stretches of DNA that have entered the host genome. DNA methylation also forms the basis of chromatin structure, which enables a single cell to grow into multiple organs or perform multiple functions. DNA methylation also plays a crucial role in the development of nearly all types of cancer.[3]
DNA methylation at the 5 position of cytosine has the specific effect of reducing gene expression and has been found in every vertebrate examined. In adult somatic cells (cells in the body, not used for reproduction), DNA methylation typically occurs in a CpG dinucleotide context; non-CpG methylation is prevalent in embryonic stem cells,[4][5][6] and has also been indicated in neural development.
Epigene “annotations” exist in all forms of life -- including plants -- and operate separately from the mutations of the nucleic instructions in the way we call “evolution.” Instead of making changes over millennia by creating populations with variations in them and then “cooking them down” by attrition of those that don’t quite fit, the epigenes are more immediate. In fact, at the one-cell microbe level, the genes and epigenes are swapped across the cell boundary so much that their merry multiplicity prevents them from going into the careful classification boxes invented by 19th century Euros. It’s a mosh pit out there. Um, down there. Uh, in there. (We’re full of ‘em.)
A starving boy in Holland during WWII.
Here’s an account of a study that threw all the strict evolutionists into a tizzy.
Summary. A historical birth cohort study of 1116 women born between August 1 1944 and April 15 1946 in the Wilhelmina Gasthuis hospital in Amsterdam, the Netherlands, was set up to study the short- and long-term effects of a limited period of extreme nutritional deprivation in the winter of 1944–1945 in the Western Netherlands. The degree of food deprivation is evidenced by a dramatic decline in third trimester pregnancy weight gain and infant birthweight. All women were traced and 84% (683/813) of survivors presently resident in the Netherlands agreed to be interviewed in their homes. There were no differences in characteristics at birth between interviewed and uninterviewed survivors. The women who were interviewed had 1299 offspring and were able to recall birthweight of all of them. Additional birthweight information from hospital and well-baby clinic (WBC) records is available for about half of the offspring. Since the famine was imposed on the entire population of a well-defined area, whose opportunities to obtain food elsewhere were severely restricted, and the women from this hospital cohort were predominantly lower middle class, the relationship between fetal nutrition and subsequent health outcomes in this cohort is not likely to be confounded by unmeasured attributes related to social class. In addition, selective losses to follow-up could be excluded, which makes the Dutch famine birth cohort a valuable resource for future studies in perinatal epidemiology.
Radiolab is an excellent way to acquire scientific sophistication because it is cheerful, funny, accessible, and rests your computer-sore eyes. Try these links:
http://www.radiolab.org/story/251876-inheritance/ This is the link for the whole sequence of stories about DNA.
http://www.radiolab.org/story/251885-you-are-what-your-grandpa-eats/ This link is for the grandpa story.
So, it appears that we’re talking about an aspect of the “epigenome” -- that is, things that affect the “expression” of the genes so that the molecular reactions that the gene encodes is different. Different chords on the keys. The mechanism is sometimes called “methylation,” which appears to be a little add-on bit, involving methane, that says, “on” or “off” or “only in certain cases.”
what goes on in seminiferous tubules
This research story above suggests that at the ages of 9 to 12, just before adolescence, a boy’s gonads are developing. Among them are the “nurse cells” in the testicles that make sperms. They are little templates for sperm. In one super-microscopic picture of them I saw, the nurse cells look as though they have their arm around the growing sperm. (It's mitosis, "budding.") In the case of the starving boys, something molecular in the template was changed that was beneficial to the results of the eventual receivers of the sperm (which were the ova in girls). These starved boys turn out to produce boys who do better than usual: fewer heart attacks, less diabetes, and so on -- both in the children and grandchildren of that man. Maybe the more vulnerable or flawed nurse cells were culled some way. No one knows.
On the other side of the gender equation, rat mom’s at McGill were distributed over a spectrum from bad-rat-mom, who rarely licks her babies, to good-rat-mom, who licks her babies all the time. The baby female rats grew up to be as maternal as their mothers. (No surprise.) Turns out that motherliness was molecular: “mom protein” (genetically controlled) is what carries signals to lick. Somehow. It turns out that it’s erotic! The licking stimulates a thyroid hormone which turns on the neurochemical serotonin ("pleasure"), which turns on bits of stuff that peel off any methylation that has been closing off some healthy genes.
http://learn.genetics.utah.edu/content/epigenetics/rats/ This is an interactive website that lets you play “mother rat.”
It turns out that “lovin’ on your babies” will make them smart, relaxed, and happy. BUT, is that any way to survive in a hostile environment? NOT. Shrewd, tense, restless rats may be the best survivors in the Darwinian sense, fit for sliding along walls in the dark and jumping-full of adrenaline at the slightest threat. Wild rats are just like that. Tame rats are not.
It's not just rats -- it's a mammal thing.
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