The Real Story on Gay Genes | DiscoverMagazine.com

Methylation turns off certain sections of genetic code. So even though we inherit two copies of every gene—one from our mother, one from our father—whether the gene is methylated often determines which of the two genes will be turned on. Methylation is inherited, just as DNA is. But unlike DNA, which has an enzyme that proofreads both the original and the copy to minimize errors, methylation has no built-in checks. It can change from one generation to the next and may be influenced by diet or environment. It’s in this mutability that Bocklandt hopes to find the secret, by seeing which flipped genetic switches correlate with homosexuality.

A linkage between DNA markers on the X chromosome an... [Science. 1993] - PubMed - NCBI

The role of genetics in male sexual orientation was investigated by pedigree and linkage analyses on 114 families of homosexual men. Increased rates of same-sex orientation were found in the maternal uncles and male cousins of these subjects, but not in their fathers or paternal relatives, suggesting the possibility of sex-linked transmission in a portion of the population. DNA linkage analysis of a selected group of 40 families in which there were two gay brothers and no indication of nonmaternal transmission revealed a correlation between homosexual orientation and the inheritance of polymorphic markers on the X chromosome in approximately 64 percent of the sib-pairs tested. The linkage to markers on Xq28, the subtelomeric region of the long arm of the sex chromosome, had a multipoint lod score of 4.0 (P = 10(-5), indicating a statistical confidence level of more than 99 percent that at least one subtype of male sexual orientation is genetically influenced.
http://healthland.time.com/2012/12/1...homosexuality/

To be specific, the new theory suggests that homosexuality is caused by epigenetic marks, or “epi-marks,” related to sensitivity to hormones in the womb. These are compounds that sit on DNA and regulate how active, or inactive certain genes are, and also control when during development these genes are most prolific. Gavrilets and his colleagues believe that gene expression may regulate how a fetus responds to testosterone, the all-important male sex hormone. They further argue that epi-marks may help to buffer a female fetus from high levels of testosterone by suppressing receptors that respond to testosterone, for example, (thus ensuring normal fetal development even in the presence of a lot of testosterone) or to buffer a male fetus from low levels of testosterone by upregulating receptors that bind to the hormone (ensuring normal fetal development even in the absence of high levels of testosterone). Normally, these epi-marks are erased after they are activated, but if those marks are passed down to the next generation, the same epi-marks that protected a man in utero may cause oversensitivity to testosterone among his daughters, and the epi-marks that protected a woman in utero may lead to undersensitivity to testosterone among her sons.