"The notion that epigenetics, rather than genetics, is the primary force promoting homosexuality sprang from several observations, explained Rice.
First, evidence shows that homosexuality can run in families. Still, only 20 percent of identical twins are both gay, said Rice. Furthermore, linkage studies looking for a genetic underpinning to sexual orientation have not turned up any “major” homosexual genes, Rice noted. “This made us suspicious that something besides genes produces heritability that isn’t genetic.” Epigenetics fits the bill.
The model focuses on the role of epigenetics in shaping how cells respond to androgen signaling, an important determinant of gonad development. The researchers suggest that androgens are also important factors in molding sexual orientation, and that various genes involved in mediating androgen signaling are regulated by epigenetic modifications. These epigenetic marks, they argue, can be passed on between generations.
As an example of how androgens shape sexuality, the researchers point to girls with congenital adrenal hyperplasia (CAH), who produce very high levels of testosterone and often display masculinized genitalia and higher rates of same-sex attraction. But testosterone levels are sometimes the same in normally developing male and female fetuses—without masculinizing the females—suggesting that something else must be playing a role.
The answer, they hypothesized, has to do with sensitivity to androgens. There are a variety of proteins that can modify androgen signaling, and the researchers hypothesize that differences in sensitivity to these signals between male and female fetuses help mediate their sexual differentiation. Rice and his colleagues suggest that such sensitivity may be regulated by the acquisition of epigenetic marks that make girls less sensitive to masculinizing androgens, or make boys more sensitive.
Such epi-marks are typically accrued early in development, as cells are programmed to become specific adult cell types. But, the researchers speculate, perhaps they could be inherited from a parent. Most epigenetic modifications are erased during development of germ cells and soon after fertilization so that cell lineages can be programmed with new epigenetic modifications. But if epi-marks that direct sexual development are not erased correctly, a mother could pass down epi-marks that direct female development to her son, resulting in an attraction to men, and vice versa for a father and his daughters, the researchers theorize.
They also expect that specific epi-marks will regulate sensitivity differently in the brain versus gonads, resulting in same-sex attraction even when normal genital development occurs, said Gavrilets."
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