The Role of Epigenetics in Homosexuality
The Role of Epigenetics in Homosexuality
The article I chose to review came from The Quarterly Review of Biology, Volume 87, No.4, pages 343-368, and is entitled, “Homosexuality as a Consequence of Epigenetically Canalized Sexual Development”, by William R. Rice, Urban Friberg, and Sergey Gavrilets.
The common occurrence of homosexuality is perplexing from an evolutionary perspective. From an evolutionary standpoint, homosexuality is a trait that would not be expected to develop and persist in the face of natural selection. Simple logic suggests that a fitness-reducing phenotype should be selected against, but homosexuality is nonetheless quite common in human populations, accounting for approximately eight to ten percent of all people. Scientists have turned again and again to genetics, especially since homosexuality has been shown to run in families, leading researchers to presume a genetic underpinning of sexual preference. However, no gene has been found for homosexuality, despite the numerous studies searching for a genetic connection.
Epigenetics – how gene expression is regulated by temporary switches, called epi-marks, appears to be a critical and overlooked factor contributing to the long-standing puzzle of why homosexuality occurs. According to the study, sex-specific epi-marks, which normally do not pass between generation and are thus “erased”, can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son. The researchers integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological model that delineates the role of epigenetics in homosexuality.
Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression. While genes hold the instructions, epi-marks (switches) direct how those instructions are carried out – when, where and how much a
The article I chose to review came from The Quarterly Review of Biology, Volume 87, No.4, pages 343-368, and is entitled, “Homosexuality as a Consequence of Epigenetically Canalized Sexual Development”, by William R. Rice, Urban Friberg, and Sergey Gavrilets.
The common occurrence of homosexuality is perplexing from an evolutionary perspective. From an evolutionary standpoint, homosexuality is a trait that would not be expected to develop and persist in the face of natural selection. Simple logic suggests that a fitness-reducing phenotype should be selected against, but homosexuality is nonetheless quite common in human populations, accounting for approximately eight to ten percent of all people. Scientists have turned again and again to genetics, especially since homosexuality has been shown to run in families, leading researchers to presume a genetic underpinning of sexual preference. However, no gene has been found for homosexuality, despite the numerous studies searching for a genetic connection.
Epigenetics – how gene expression is regulated by temporary switches, called epi-marks, appears to be a critical and overlooked factor contributing to the long-standing puzzle of why homosexuality occurs. According to the study, sex-specific epi-marks, which normally do not pass between generation and are thus “erased”, can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son. The researchers integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological model that delineates the role of epigenetics in homosexuality.
Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression. While genes hold the instructions, epi-marks (switches) direct how those instructions are carried out – when, where and how much a
References: Rice WR, Friberg U, Gavrilets S. Homosexuality as a consequence of epigenetically canalized sexual development. The Quarterly Review of Biology, 11 Dec 2012. Online.