Early life stress affects the transcription and chromatin accessibility of spermatogonial cells
Adversity in early life has lasting effects on the physiology and behavior of exposed individuals and their descendants. In mice, early-life stress alters the RNA content of adult sperm, and this RNA is sufficient to transmit some of the effects to the offspring who were never exposed. However, sperm cells are not yet formed during the early postnatal window in which the exposure occurs.…
Early-life stress has enduring physiological and behavioral impacts on exposed individuals and their offspring, as observed in mice. Although sperm cells have not yet developed during the early postnatal exposure phase, spermatogonial cells (SPGs) arise at that time. The question remained whether SPGs would react to the stress and preserve its molecular signature into adulthood.
The study reveals that early-life stress impacts both the transcriptome and chromatin accessibility of mouse SPGs. One day following the cessation of exposure, a significant transcriptional reaction was observed, with proliferation and nucleosome-organization programs being upregulated synchronously. However, in adulthood, the transcriptional response was comparatively subtle and primarily featured downregulated gene programs.
Through single-cell profiling of the entire testis, the adult response was localized to spermatogonial stem cells (SSCs) and genes implicated in spermatogenesis. At the chromatin level, accessibility alterations occurred one day after exposure at signal-responsive transcription factor families' binding motifs. In adulthood, these changes manifested at a different set of families, specifically at primed enhancers.
These findings establish SPGs as potential sources of molecular alterations later detected in adult sperm, following early postnatal environmental exposure.
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