Epigenetics and homosexuality

Is homosexuality genetic? It’s a long-running debate.

Now researchers at the University of Tennessee (UT), Knoxville, say they’ve found a clue that may unlock the mystery. It lies in how gene expression is regulated by temporary switches, ie, epigenetics.

A working group at the National Institute for Mathematical and Biological Synthesis (NIMBioS), based at UT, used mathematical modelling that found the transmission of sex-specific epi-marks may signal homosexuality.

According to the study, published in The Quarterly Review of Biology, sex-specific epi-marks, which are ‘erased’ and thus normally do not pass between generations, can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son.

“Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference,” said Sergey Gavrilets, paper co-author, joint professor of math and ecology and evolutionary biology, and NIMBioS’s associate director for scientific activities. “However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection.”

Epi-marks may be the trigger they’ve been searching for.

Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression. While genes hold the instructions, epi-marks direct how those instructions are carried out. They are usually produced anew each generation, but recent evidence demonstrates that they sometimes carry over between generations.

Sex-specific epi-marks produced in early foetal development protect each sex from the substantial natural variation in testosterone that occurs during later foetal development. Different epi-marks protect different sex-specific traits from being masculinised or feminised.

The researchers found homosexuality can occur in opposite-sex offspring when the sex-specific epi-marks are carried on to another generation.

“We discovered when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminisation of some traits in sons, such as sexual preference, and similarly a partial masculinisation of daughters,” said Gavrilets.

In their study, the researchers integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological and mathematical model that delineates the role of epigenetics in homosexuality.

“The study solves the evolutionary riddle of homosexuality, finding that ‘sexually antagonistic’ epi-marks, which normally protect parents from natural variation in sex hormone levels during foetal development, sometimes carry over across generations and cause homosexuality in opposite-sex offspring,” said Gavrilets.

The mathematical modelling demonstrates that gene coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring.

“Transmission of sexually antagonistic epi-marks between generations is the most plausible evolutionary mechanism of the phenomenon of human homosexuality,” said Gavrilets.

The paper is co-authored with William Rice, a professor at the University of California, Santa Barbara, and Urban Friberg, a professor at Uppsala University in Sweden.