Dec 12, 2012 Comments Off Chuck Biscuits
Excerpted from i09: A team of international researchers has completed a study that suggests we will probably never find a ‘gay gene.’ Sexual orientation is not about genetics, say the researchers, it’s about epigenetics. This is the process where DNA expression is influenced by any number of external factors in the environment. And in the case of homosexuality, the researchers argue, the environment is the womb itself.
The Epigenetic Key
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.
Masculinization and Feminization
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.”
The resulting model predicted that homosexuality can be produced by transgenerational epigenetic inheritance.
Normally, sex-specific marks that are triggered during early fetal development work to protect boys and girls in the womb from undergoing too much natural variation in testosterone, which should normally happen later in a pregnancy. Epigenetic processes prevent female fetuses from becoming masculinized when testosterone exposure gets too high, and vice versa for males.
Moreover, epi-marks also protect different sex-specific traits from swinging in the opposite direction; some affect the genitals, and others may affect sexual orientation. These epi-marks can be transmitted across generations from fathers to daughters, or mothers to sons.
Essentially, Rice and Friberg believe they have discovered the presence of “sexually antagonistic” epi-marks — which sometimes carry over to the next generation and cause homosexuality in opposite-sex offspring.
And importantly — in order to satisfy the rules of Darwinian selection — the researchers noted through their mathematical modeling that these epigenetic characteristics can easily proliferate in the population because they increase the fitness of the parent; these epi-marks normally protect parents from natural variation in sex hormone levels during fetal development. They only rarely reduce the fitness of offspring.