Researchers looking for a genetic signature of homosexuality have been barking up the wrong tree, according to a trio of researchers in the United States and Sweden. Instead, the scientists posit, epigenetic influences acting on androgen signaling in the brain may underlie sexual orientation.
In a paper published last week December 11 in The Quarterly Review of Biologythey propose a model describing how epigenetic markers that steer sexual development in males could promote homosexual orientation in females, and vice versa.
Indeed, Andrea Cianian evolutionary psychologist at the University of Padova, thinks that a variety of factors, including genes and epigenetics, influence sexual orientation. The model was developed by William Ricean evolutionary geneticist at the University of California, Santa Barbara; Sergey Gavriletsa mathematician at the University of Tennessee; and Urban Fribergan evolutionary biologist at the University of Uppsala.
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. 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 Epigenetic roots of homosexuality in japan 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 CAHwho 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 Epigenetic roots of homosexuality in japan 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. Determining whether epi-marks have not been erased will be difficult to test, said Vilain, because the marks relevant to sexual orientation will probably be in the brain.
But Rice proposes that because homosexuality can run in families, surveying the epigenomes of sperm from men with or without lesbian daughters could reveal key differences. Is it important for us to know?
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What About Climate Change? In Western countries today, the prevalence of male homosexuality is. All of these findings point toward a prenatal epigenetic origin for the.