
In the developing mammalian testis, only a small proportion of fetal and neonatal prospermatogonia give rise to the foundational pool of spermatogonial stem cells (SSCs). The article suggests that differential epigenetic programming contributes to the molecular mechanisms by which an early subset of developing prospermatogonia becomes predetermined to form the foundational pool of SSCs. This would include epigenetic programming that promotes active expression of genes needed to develop advantageous characteristics, as well as differential epigenetic priming which bookmarks genes that comprise the SSC‐specific transcriptome to become activated when foundational SSCs appear in the postnatal testis.
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