A controversial study was recently released that suggest epigenetics and not genetics, underlies homosexuality.
Epigenetics defines how gene expression is regulated by temporary switches called epi-marks or those extra layers of information that control how certain genes are expressed. The study concludes that these epi-marks are critical and sometimes overlooked factor contributing to the long-standing puzzle of why homosexuality occurs.
Published online in “The Quarterly Review of Biology,” the study added that sex-specific epi-marks, which normally do not pass between generations and are "erased," can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son.
Sex-specific epi-marks produced in early fetal development protect each sex from the substantial natural variation in testosterone that occurs during later fetal development. Sex-specific epi-marks stop girl fetuses from becoming masculine when they experience atypically high testosterone, and vice versa for boy fetuses.
Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and similarly a partial masculinization of daughters.
The study solves the evolutionary riddle of homosexuality. It finds that "sexually antagonistic" epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring.
The mathematical modelling demonstrates that genes 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.
The study further that homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection. Homosexuality is nevertheless common for men and women in most cultures.
Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference. However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection.
The paper's authors are Catherine Crawley, William Rice and Urban Friberg, professors from different institutions and working for the National Institute for Mathematical and Biological Synthesis (NIMBioS). The institute brings together researchers from around the world to collaborate across disciplinary boundaries to investigate solutions to basic and applied problems in the life sciences.
NIMBioS is sponsored by the National Science Foundation, the U.S. Department of Homeland Security, and the U.S. Department of Agriculture with additional support from The University of Tennessee, Knoxville.
In the study, the authors 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.
Epigenetics defines how gene expression is regulated by temporary switches called epi-marks or those extra layers of information that control how certain genes are expressed. The study concludes that these epi-marks are critical and sometimes overlooked factor contributing to the long-standing puzzle of why homosexuality occurs.
Published online in “The Quarterly Review of Biology,” the study added that sex-specific epi-marks, which normally do not pass between generations and are "erased," can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son.
Sex-specific epi-marks produced in early fetal development protect each sex from the substantial natural variation in testosterone that occurs during later fetal development. Sex-specific epi-marks stop girl fetuses from becoming masculine when they experience atypically high testosterone, and vice versa for boy fetuses.
Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and similarly a partial masculinization of daughters.
The study solves the evolutionary riddle of homosexuality. It finds that "sexually antagonistic" epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring.
The mathematical modelling demonstrates that genes 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.
The study further that homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection. Homosexuality is nevertheless common for men and women in most cultures.
Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference. However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection.
The paper's authors are Catherine Crawley, William Rice and Urban Friberg, professors from different institutions and working for the National Institute for Mathematical and Biological Synthesis (NIMBioS). The institute brings together researchers from around the world to collaborate across disciplinary boundaries to investigate solutions to basic and applied problems in the life sciences.
NIMBioS is sponsored by the National Science Foundation, the U.S. Department of Homeland Security, and the U.S. Department of Agriculture with additional support from The University of Tennessee, Knoxville.
In the study, the authors 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.
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