lunedì 17 dicembre 2012


Why Evolution Hasn’t Selected Against Homosexuality
12/13/2012 Sarah C.P. Williams
An interdisciplinary team proposes that sexual orientation is inherited epigenetically. What evidence supports this theory? Find out...

The molecular underpinning of human sexuality, including homosexuality, could lie in the inheritance of epigenetic marks, according to a paper published this week that provides a step-by-step argument for the idea (1). The theory is not yet backed by epigenetic data on people with different sexual orientations. Instead, it relies on established findings on the frequency of homosexuality and the known mode of inheriting epigenetic marks to make its case.
The molecular underpinning of human sexuality, including homosexuality, could lie in the inheritance of epigenetic marks, according to a new paper. Source: Wikimedia Commons, Bob J. Galindo

An interdisciplinary team of evolutionary biologists and mathematicians brought together by the National Institute for Mathematical and Biological Synthesis was studying genomic conflict—what happens when genes inherited by someone are not aligned—when the topic of homosexuality came up. Since homosexuality decreases a person’s odds of passing on the trait to future generations through reproduction, biologists have had difficulty explaining why it hasn’t been selected against by evolution.
“It’s one of the riddles of biology,” said William Rice, an evolutionary biologist at the University of California, Santa Barbara and author of the study that published in The Quarterly Review of Biology. “What we are trying to do is explain an enigmatic phenotype from an evolutionary standpoint.”

The team brainstormed solutions to the puzzle, and soon began to converge on a theory based in epigenetics. “The idea that epigenetics might contribute to homosexuality has been around for a long time,” said Rice. “But there was no coherent theory, no empirical support.”

The crux of the theory is that in the womb, sex and sexuality are influenced by levels of testosterone. But this isn’t just mediated by whether a fetus had male or female genes that control the level of testosterone production. Epigenetic marks on the genome also control how the fetus—and later, the child and adult—responds to testosterone levels. Most male fetuses have epi-marks that make them more sensitive to testosterone than female fetuses.

Usually, such epi-marks are erased from the egg and sperm and re-established in a fetus. But Rice’s team argues that when male epi-marks are not erased from sperm and inherited by a daughter, or when female epi-marks from an egg are inherited by a son, sexuality could be influenced. The change in the fetus’ reaction to testosterone is not enough to change their sex, but could alter their sexuality.

Some popular media articles this week have claimed that this new finding nixes the idea of a “gay gene.” But researchers had already realized that sexuality is not likely to be controlled by one, Mendelian gene mutation and have been looking at more complex factors. And this study certainly does not close the book on the biology of homosexuality.

“We definitely need further experiments to confirm this theory,” said Rice. “And in the paper, we provide a way to test it, by doing genome-wide epigenetic profiling of dads with and without lesbian daughters to find differences.”

Even the discovery of those epigenetic marks will not fully explain the biology of sexual orientation, explained Rice. It could just be one possible inheritance mode of a complex phenotype.


1. Rice WR, Friberg U, Gavrilets S. Homosexuality as a consequence of epigenetically canalized sexual development. 2012. The Quarterly Review of Biology 87:4.


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