Developmental Biology Center and Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
University of Minnesota Masonic Cancer Center, Minneapolis, Minnesota, United States of America.
PLoS Genet. 2022 Feb 22;18(2):e1010088. doi: 10.1371/journal.pgen.1010088. eCollection 2022 Feb.
The mammalian nuclear hormone receptors LRH1 (NR5A2) and SF1 (NR5A1) are close paralogs that can bind the same DNA motif and play crucial roles in gonadal development and function. Lrh1 is essential for follicle development in the ovary and has been proposed to regulate steroidogenesis in the testis. Lrh1 expression in the testis is highly elevated by loss of the sex regulator Dmrt1, which triggers male-to-female transdifferentiation of Sertoli cells. While Sf1 has a well-defined and crucial role in testis development, no function for Lrh1 in the male gonad has been reported. Here we use conditional genetics to examine Lrh1 requirements both in gonadal cell fate reprogramming and in normal development of the three major cell lineages of the mouse testis. We find that loss of Lrh1 suppresses sexual transdifferentiation, confirming that Lrh1 can act as a key driver in reprogramming sexual cell fate. In otherwise wild-type testes, we find that Lrh1 is dispensable in Leydig cells but is required in Sertoli cells for their proliferation, for seminiferous tubule morphogenesis, for maintenance of the blood-testis barrier, for feedback regulation of androgen production, and for support of spermatogenesis. Expression profiling identified misexpressed genes likely underlying most aspects of the Sertoli cell phenotype. In the germ line we found that Lrh1 is required for maintenance of functional spermatogonia, and hence mutants progressively lose spermatogenesis. Reduced expression of the RNA binding factor Nxf2 likely contributes to the SSC defect. Unexpectedly, however, over time the Lrh1 mutant germ line recovered abundant spermatogenesis and fertility. This finding indicates that severe germ line depletion triggers a response allowing mutant spermatogonia to recover the ability to undergo complete spermatogenesis. Our results demonstrate that Lrh1, like Sf1, is an essential regulator of testis development and function but has a very distinct repertoire of functions.
哺乳动物核激素受体 LRH1(NR5A2)和 SF1(NR5A1)是紧密的同源物,它们可以结合相同的 DNA 基序,并在性腺发育和功能中发挥关键作用。LRH1 对卵巢中的卵泡发育至关重要,并且据推测可以调节睾丸中的类固醇生成。缺失性别调节剂 Dmrt1 会导致睾丸中 Sertoli 细胞的雄性到雌性转分化,从而使睾丸中 Lrh1 的表达高度升高。虽然 Sf1 在睾丸发育中具有明确且关键的作用,但尚未报道 Lrh1 在雄性性腺中的功能。在这里,我们使用条件遗传学来检查 Lrh1 在性腺细胞命运重编程和正常发育中的要求,分别涉及小鼠睾丸的三个主要细胞谱系。我们发现 Lrh1 的缺失抑制了性转分化,证实了 Lrh1 可以作为重编程性细胞命运的关键驱动因素。在其他方面为野生型的睾丸中,我们发现 Lrh1 在 Leydig 细胞中是可有可无的,但在 Sertoli 细胞中对于它们的增殖、生精小管形态发生、血-睾屏障的维持、雄激素产生的反馈调节以及支持精子发生是必需的。表达谱分析确定了可能是大多数 Sertoli 细胞表型的基础的异常表达基因。在生殖系中,我们发现 Lrh1 对于维持功能性精原细胞是必需的,因此突变体逐渐失去精子发生。RNA 结合因子 Nxf2 的表达降低可能导致 SSC 缺陷。然而,出乎意料的是,随着时间的推移,Lrh1 突变体生殖系恢复了丰富的精子发生和生育能力。这一发现表明,严重的生殖系耗竭会触发一种反应,使突变体精原细胞恢复完全精子发生的能力。我们的结果表明,LRH1 与 Sf1 一样,是睾丸发育和功能的必需调节剂,但具有非常不同的功能谱。