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Epigenetic theories of homosexuality : ウィキペディア英語版 | Epigenetic theories of homosexuality
Epigenetic theories of homosexuality concerns the studies of changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence, and their role in the development of homosexuality. Epigenetics examines the set of chemical reactions that switch parts of the genome on and off at strategic times and locations in the organism's life cycle. Instead of affecting the organism's DNA sequence, non-genetic factors cause the organism’s genes to express themselves differently. DNA in the human body is wrapped around histones, which are proteins that package and order DNA into structural units. DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome.〔("The Epigenome at a Glance." ) Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013. 〕 It tightly wraps inactive genes on the DNA sequence making those genes unreadable while loosely wrapping active genes making them more expressive. The more tightly wrapped the gene, the less it will be expressed in the organism. These epigenetic tags react to stimuli presented from the outside world. It adjusts specific genes in the genome to respond to humans' rapidly changing environments. The idea of epigenetics and gene expression has been a theory applied to the origins of homosexuality in humans. One team of researchers examined the effects of epi-marks buffering XX fetuses and XY fetuses from certain androgen exposure and used published data on fetal androgen signaling and gene regulation through non-genetic changes in DNA packaging to develop a new model for homosexuality.〔Richards, Sabrina. ("Can Epigenetics Explain Homosexuality?." ) The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.〕 The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert sexual preference in individuals without altering genitalia or sexual identity.〔"National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.〕 This research gives support to the hypothesis that homosexuality stems from the under expression of certain genes on the DNA sequence involved with sexual preferences. This theory as well as other concepts involved with epi-marks, twin studies, and fetal androgen signaling will be explored here. == Epigenetic marks ==
Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. Moreover, epi-marks are modifications of histone proteins.〔Ruthenburg, A., C. Allis, and J. Wysocka. "Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark." Molecular Cell 25.1 (2007): 15-30. Print. 〕 Epigenetic marks are modifications of the methyl and acetyl groups that bind to DNA histones thereby changing how the proteins function and as a result, alter gene expression.〔Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis〕 Epi-marks change how the histones function and as a result, influence the way genes are expressed.〔Friberg, Urban, Sergey Gavrilets, and William R. Rice. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology 87.4 (2012): n. pag. Print. 〕 Epigenetic marks are intended to promote normal sexual development while in fetal development, however, they can be passed on to offspring through the process of mitosis. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to masculinization of female offspring and feminization of male offspring.〔("Gene Regulation May Explain How Homosexuality Flourishes." ) LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.〕 However, these epi-marks hold no consistency between individuals in regard to strength and variability.
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