The TGF-β/SMAD Signaling Pathway Prevents Follicular Atresia by Upregulating MORC2

In mammals, female fertility is determined by the outcome of follicular development (ovulation or atresia). The TGF-beta/SMAD signaling pathway is an important regulator of this outcome. However, the molecular mechanism by which the TGF-beta/SMAD signaling pathway regulates porcine follicular atresia has not been fully elucidated. Microrchidia family CW-type zinc finger 2 (MORC2) is anovel epigenetic regulatory protein widely expressed in plants, nematodes, and mammals. Our previous studies showed that MORC2 is a potential downstream target gene of the TGF-beta/SMAD signaling pathway. However, the role of MORC2 in porcine follicular atresia is unknown. To investigate this, qRT-PCR, western blotting, and TdT-mediated dUTP nick-end labeling were performed. Additionally, the luciferase activity assay was conductedto confirm that the TGF-beta/SMAD signaling pathway regulates MORC2. Our results demonstrate that MORC2 is animportant anti-apoptotic molecule that prevents porcine follicular atresia via a pathway involving mitochondrial apoptosis, not DNA repair. Notably, this studyrevealsthat the TGF-beta/SMAD signaling pathway inhibits porcine granulosa cell apoptosis by up-regulating MORC2. The transcription factor SMAD4 regulated the expression of MORC2 by binding to its promoter. Our results will help to reveal the mechanism underlying porcine follicular atresia and improve the reproductive efficiency of sows.

Automated summary

The article translated introduces the regulatory role of the TGF-beta/SMAD signaling pathway in porcine follicular atresia and the important role of MORC2 in it. The results of the study reveal that MORC2 prevents porcine follicular atresia through the pathway involving mitochondrial apoptosis instead of DNA repair, and the TGF-beta/SMAD signaling pathway inhibits porcine granulosa cell apoptosis by up-regulating MORC2. SMAD4 is the transcription factor that regulates the expression of MORC2.