Department of Ecology, Evolution & Marine Biology, University of California, Santa Barbara, CA, USA.
Bioessays. 2013 Sep;35(9):764-70. doi: 10.1002/bies.201300033. Epub 2013 Jul 19.
We recently synthesized and reinterpreted published studies to advance an epigenetic model for the development of homosexuality (HS). The model is based on epigenetic marks laid down in response to the XX vs. XY karyotype in embryonic stem cells. These marks boost sensitivity to testosterone in XY fetuses and lower it in XX fetuses, thereby canalizing sexual development. Our model predicts that a subset of these canalizing epigenetic marks stochastically carry over across generations and lead to mosaicism for sexual development in opposite-sex offspring--the homosexual phenotype being one such outcome. Here, we begin by outlining why HS has been under-appreciated as a commonplace phenomenon in nature, and how this trend is currently being reversed in the field of neurobiology. We next briefly describe our epigenetic model of HS, develop a set of predictions, and describe how epigenetic profiles of human stem cells can provide for a strong test of the model.
我们最近综合并重新解释了已发表的研究，以推进同性恋（HS）发展的表观遗传学模型。该模型基于胚胎干细胞对 XX 与 XY 染色体组的表观遗传标记，这些标记提高了 XY 胚胎对睾丸激素的敏感性，降低了 XX 胚胎的敏感性，从而对性发育进行了疏导。我们的模型预测，这些疏导性的表观遗传标记中有一部分会随机跨越几代人，并导致性发育的镶嵌现象，即相反性别的后代出现同性恋表型。在这里，我们首先概述为什么 HS 作为自然界中的一种常见现象一直未被充分认识，以及这种趋势在神经生物学领域是如何被逆转的。接下来，我们简要描述了我们的 HS 表观遗传学模型，提出了一系列预测，并描述了人类干细胞的表观遗传特征如何为该模型提供强有力的检验。
