Primordial follicle activation is affected by the absence of Sohlh1 in mice

Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1−/− mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial‐to‐primary follicle transition in Sohlh1−/− mouse ovaries. However, detailed analyses of these phenomena have not been performed. In this study, we used Sohlh1−/− transgenic mice to explore the role of Sohlh1 in folliculogenesis. The results showed that only primordial follicles and empty follicles can be observed in Sohlh1−/− ovaries from 0.5 to 23.5 dpp. The expression of Foxo3 and FOXO3 was downregulated; nucleocytoplasmic shuttling of FOXO3 was normal in 7.5‐dpp Sohlh1+/+ but not Sohlh1−/− ovaries; and primordial follicle activation (PFA) was not observed in 7.5‐dpp Sohlh1−/− mice. The expression levels of KIT, AKT, and P308‐AKT were downregulated (p 0.05). The KIT/PI3K/AKT pathway was inhibited. Furthermore, we conducted a dual luciferase assay and chromatin immunoprecipitation. The results showed that SOHLH1 can upregulate the Kit gene by binding to the −3698 bp E‐box motif. The absence of Sohlh1 may affect PFA in mouse ovaries via downregulation of Kit and inhibition of the KIT/PI3K/AKT pathway. The absence of spermatogenesis‐ and oogenesis‐specific basic helix‐loop‐helix 1 (SOHLH1) can influence folliculogenesis by affecting primordial follicle activation in the ovaries, and can lead to disruption of the KIT/PI3K/AKT/FOXO3 pathway. SOHLH1 can control Kit by binding to −3698 E‐box site.