PARL regulates porcine oocyte meiotic maturation by mediating mitochondrial activity

Abstract

PARL is a rhomboid membrane protein that plays a crucial role in regulating the metabolism and maintaining the homeostasis of mitochondria which provide important energy and material reserves for oocyte maturation. However, the impact of PARL on oocyte maturation remains poorly understood. Here, we elucidated the pivotal role of PARL in oocyte maturation through its regulatory effects on mitochondrial activity. Specifically, our findings revealed that inhibiting PARL expression by interfering with RNA transcription in oocytes led to a substantial decrease in the rate of first polar body extrusion and early development of parthenogenetically activated embryos. Moreover, PARL deficiency disrupted mitochondrial distribution and activity, leading to the accumulation of ROS, abnormal distribution of CGs and actin, increased tubulin acetylation modification, disturbed spindle assembly and chromosome alignment, ultimately caused DNA damage in porcine oocytes at the metaphase II stage. Intriguingly, PARL deficiency did not cause occurrence of apoptosis in oocytes. Furthermore, our study highlighted that PARL deficiency caused the aberrant expression of genes associated with oocyte maturation, particularly those genes associated with mitochondrial function and DNA integrity. Collectively, these results demonstrate that the indispensable role of PARL in orchestrating porcine oocyte meiotic maturation though its modulation of mitochondrial activity.