Rethinking sex determination of non-gonadal tissues

被引：40
作者：
Arnold, Arthur P. [1 ]
机构：
[1] Univ Calif Los Angeles, Brain Res Inst, Neuroendocrinol Lab, Dept Integrat Biol & Physiol, Los Angeles, CA 90024 USA
来源：
SEX DETERMINATION IN VERTEBRATES | 2019年 / 134卷
关键词：
DIMORPHIC GENE-EXPRESSION; X-CHROMOSOME INACTIVATION; Y-CHROMOSOME; DOSAGE COMPENSATION; STROKE SENSITIVITY; MOUSE MODELS; COMPLEMENT; BRAIN; EVOLUTION; HORMONES;
D O I：
10.1016/bs.ctdb.2019.01.003
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Evolution of genetic mechanisms of sex determination led to two processes causing sex differences in somatic phenotypes: gonadal differentiation and sex chromosome dosage inequality. In species with heteromorphic sex chromosomes, the sex of the individual is established at the time of formation of the zygote, leading to inherent sex differences in expression of sex chromosome genes beginning as soon as the embryonic transcriptome is activated. The inequality of sex chromosome gene expression causes sexual differentiation of the gonads and of non-gonadal tissues. The difference in gonad type in turn causes lifelong differences in gonadal hormones, which interact with unequal effects of X and Y genes acting within cells. Separating the effects of gonadal hormones and sex chromosomes has been possible using mouse models in which gonadal determination is separated from the sex chromosomes, allowing comparison of XX and XY mice with the same type of gonad. Sex differences caused by gonadal hormones and sex chromosomes affect basic physiology and disease mechanisms in most or all tissues.
引用
收藏
页码：289 / 315
页数：27
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