Abstract
In mammals, sex chromosomes start to program autosomal gene expression and epigenetic patterns very soon after fertilization. Yet whether the resulting sex differences are perpetuated throughout development and how they connect to the sex-specific expression patterns in adult tissues is not known. There is a dearth of information on the timing and continuity of sex biases during development. It is also unclear whether sex-specific selection operates during embryogenesis. On the other hand, there is mounting evidence that all adult tissues exhibit sex-specific expression patterns, some of which are independent of hormonal influence and due to intrinsic regulatory effects of the sex chromosome constitution. There are many diseases with origins during embryogenesis that also exhibit sex biases. Epigenetics has provided us with viable mechanisms to explain how the genome stores the memory of developmental events. We propose that some of these marks can be traced back to the sex chromosomes, which interact with the autosomes and establish sex-specific epigenetic features soon after fertilization. Sex-biased epigenetic marks that linger after reprograming may reveal themselves at the transcriptional level at later developmental stages and possibly, throughout the lifespan. Detailed molecular information on the ontogeny of sex biases would also elucidate the sex-specific selective pressures operating on embryos and how compensatory mechanisms evolved to resolve sexual conflict.
Highlights
In the age of genomics, it has become ever more obvious that the long-known differences between males and females in health, longevity, disease risk and presentation, and response to therapy have genetic and epigenetic foundations (Yang et al, 2006; Isensee et al, 2008; Singmann et al, 2015; Chen et al, 2016; Mayne et al, 2016; Gershoni and Pietrokovski, 2017; McCormick et al, 2017)
The driver of sex differences in mammals has traditionally been considered to be the socalled sex determination pathway, sex-specific transcriptional and epigenomic profiles are present in the embryo very soon after fertilization in a range of mammals, i.e., well before the development
Long before sex hormones appear, the primary sex-determining factor is the imbalance in sex chromosome composition (Blecher and Erickson, 2007; Arnold, 2012)
Summary
In the age of genomics, it has become ever more obvious that the long-known differences between males and females in health, longevity, disease risk and presentation, and response to therapy have genetic and epigenetic foundations (Yang et al, 2006; Isensee et al, 2008; Singmann et al, 2015; Chen et al, 2016; Mayne et al, 2016; Gershoni and Pietrokovski, 2017; McCormick et al, 2017). On the other hand, implantation erases all sex biases between XX and XY embryos, there are still genes encoded on the sex chromosomes that are differentially expressed before the appearance of sex hormones that could lead to sex-biased autosomal gene expression Such is the case of Y-linked genes, absent in female cells, X-linked allelic variants and genes that escape XCI altogether (Disteche and Berletch, 2015). Detailed molecular information across all stages of development for males and females would allow us to test the major hypotheses on the ontogeny and evolutionary significance of sex biases by integrating functional studies of individual genes with systems-level analyses and identifying similarities and differences across a range of species
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