Epigenetics

Last night I was at a party at the home of SF writer Craig DeLancey, and the question of epigenetics came up. (I have to tell you, parties among writers/scientists are the only venues this sort of thing comes up for me. It doesn't happen, for instance, at meetings of the Home Owners' Association.) I was familiar with the basic idea of epigenetics, which is that having genes isn't the whole story; the greater part is how, when, how often, and in what order those genes are switched on or off during the development of an organism. Some of the mechanisms by which this is done (such as methylation) are becoming well understood. The overall reasons, as yet, are mostly not.

The cool part, however, is that the changes inside the cell caused by epigenetics can be inheritable, in at least three ways. Two of them I was aware of before last night's party; the other one I was not.

First, as everybody knows, stem cells have the complete genome encased in each cell. Stem cells develop into various kinds of cells by switching on, say, the brain-developing genes and switching off the toe-developing genes. As these newly differentiated cells divide, the switching-on-or-off carries into the two resulting daughter cells, ensuring that you don't get a toe inside your brain. This is Epigenesis I.

In Epigenesis II, adult cells that divide also bequeath their switched-on-or-off pattern to daughter cells. Thus, not only do insulin-processing cells beget more insulin-processing cells, if yours are doing a lousy job of this task, so will your new ones. This epigenesis is thought to be the result of the transference of existing cell structures in the two dividing cells, as well as of any genes that may be malfunctioning. No real surprise here.

The surprise comes in Epigenesis III. Some traits acquired in mothers as a result of how their patterns of cells react to environmental toxins seems to be inherited by their offspring. This sounds almost LaMarckian, but there is proof from experiments with agouti mice. Mice with identical genomes (they were clones) were exposed to high concentrations of BPA (that's the same toxin being yelled about with regard to plastic water bottles). The offspring of those so exposed were a different color (yellow rather than brown) and gained weight easily. This might have been construed as damage to their genomes -- except that the new offspring were then not exposed to any more BPA, and still their offspring showed heritable patterns of color and weight gain, presumably as a result of the passing on of Gen II's epigenetic patterns. And the abnormalities were reversed by feeding the mice diets high in soy, indicating they were not set-in-stone genetic instructions.

This boggles my mind. Not only does it shift everything I thought I knew about genes, it also lends terrible weight to that most Biblical of curses: The sins of the fathers shall be passed onto the children, unto the fourth generation.

Other than disturbing my mind -- or maybe because of it -- it was a terrific party.