Spermatogenesis relies on exquisite stem cell homeostasis, the carefully balanced self-renewal and differentiation of spermatogonial stem cells (SSCs). Disturbing this equilibrium will likely manifest through sub- or infertility, a global health issue with often idiopathic presentation. In this respect, disease phenotypes caused by haploinsufficiency of otherwise vital developmental genes are of particular interest. Here, we show that mice heterozygous for Trim28, an essential epigenetic regulator, suffer gradual testicular degeneration. Contrary to previous reports we detect Trim28 expression in spermatogonia, albeit at low levels. Further reduction through Trim28 heterozygosity increases the propensity of SSCs to differentiate at the cost of self-renewal.

精子发生依赖于精干细胞稳态，精平衡的自我更新和精原干细胞（SSCs）的分化。破坏这种平衡很可能会通过不孕或不孕症来体现，这是一种普遍存在自发性表现的全球性健康问题。在这方面，由其他重要的发育基因的单倍不足引起的疾病表型特别令人关注。在这里，我们显示了Trim28（必需的表观遗传调控因子）杂合子的小鼠睾丸逐渐退化。与以前的报告相反，我们检测到精子中Trim28的表达，尽管其水平较低。通过Trim28杂合性进一步降低，会增加SSC分化的倾向，而这是以自我更新为代价的。