Schematic diagram of the sex differences in the development of human pre-gastrulation embryos. (IMAGE)
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The distinct parental origins of the X chromosome lead to X-specific lower methylation in female embryos (at least in TE lineage), which, combined with the incomplete X chromosome inactivation and sex-specific cell-cell communications, contributes to the sex-differential transcription and development. These include 1) the differentiation advantage towards CTBs, more active cell cycle, enhanced mitochondrial function, stronger vasculogenesis signals, and higher immunotolerance potentials in the female TE lineage, and the differentiation advantage towards STBs and stronger hormone-secreting function in the male TE lineage; 2) the higher proliferation potential and differentiation advantage towards AVE in the male PE lineage; and 3) the higher proliferation potential in male EPI lineage. These differences may serve as the underlying cause for the sex-differential development of the embryos/fetuses, with males prioritizing fetoplacental growth and females tending to ensure resilience to damage. EPI, epiblast. PE, primitive endoderm. TE, trophectoderm. XCI, X chromosome inactivation. AVE, anterior visceral endoderm. CTB, cytotrophoblast. STB, syncytiotrophoblast.
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