It’s an argument that has found some traction in anti-gay movements that want to label homosexuality as a “curable affliction”, but a group of scientists have new evidence that there isn’t a “gay gene”, but that it’s about epigenetics, or genetic traits that are expressed through external factors, mainly from within the womb. In a nutshell, it means that the traits that express themselves are genetic and can be passed down, but there isn’t a single gene or exact gene sequence that in and of itself causes homosexuality.
Writing in The Quarterly Review of Biology, researchers William Rice, a professor at the University of California, Santa Barbara, and Urban Friberg, a professor at Uppsala University in Sweden, believe that homosexuality can be explained by the presence of epi-marks — temporary switches that control how our genes are expressed during gestation and after we’re born.
Specifically, the researchers discovered sex-specific epi-marks which, unlike most genetic switches, get passed down from father to daughter or mother to son. Most epi-marks don’t normally pass between generations and are essentially “erased.” Rice and Friberg say this explains why homosexuality appears to run in families, yet has no real genetic underpinning.
Epigenetic mechanisms can be seen as an added layer of information that clings to our DNA. Epi-marks regulate the expression of genes according to the strength of external cues. Genes are basically the instruction book, while epi-marks direct how those instructions get carried out. For example, they can determine when, where, and how much of a gene gets expressed.
Moreover, epi-marks are usually produced from scratch with each generation — but new evidence is showing that they can sometimes carryover from parent to child. It’s this phenomenon that gives the impression of having shared genes with relatives.
To reach this conclusion, Rice and Friberg created a biological and mathematical model that charted the role of epigenetics in homosexuality. They did so by applying evolutionary theory to recent advances in the molecular regulation of gene expression and androgen-dependent sexual development.
This data was integrated with recent findings from the epigenetic control of gene expression, especially in embryonic stem cells. This allowed the researchers to develop and empirically support a mathematical model of epigenetic-based canalization of sexual development, or the tendency of heredity to restrict the development of some characteristics to just one or a few traits. Their model successfully predicted the evolution of homosexuality in both sexes when canalizing epi-marks carry over across generations with nonzero probability.
In their study, the team writes that they “tracked changes in chromatin structure that influence the transcription rate of genes (coding and noncoding, such as miRNAs), including nucleosome repositioning, DNA methylation, and/or modification of histone tails, but not including changes in DNA sequence.”
Submitted by Delsyd
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