Dnajc5b contributes to male fertility by maintaining the mitochondrial functions and autophagic homeostasis during spermiogenesis
》》Journal：Cellular and Molecular Life Sciences
》》相关产品：CCCP (SJ-MX4008) 和 Chloroquine (SJ-MA0048A)
》》产品引用描述：
》》Abstract：
DnaJ heat shock protein family member C5 beta (DNAJC5B), also known as cysteine-string protein beta, exhibits a prominent expression in testicular tissue and plays an important role in acrosomal exocytosis in vitro. Nevertheless, the precise role and underlying mechanism of DNAJC5B in spermatogenesis and male fertility remain poorly understood. The meta-analysis of RNA-sequencing datasets from porcine and murine testes reveals that Dnajc5b could be a pivotal factor in spermatogenesis. This study illustrates that male fertility declines with an increased ratio of abnormal spermatozoa in germ-cell knockout Dnajc5b mice. DNAJC5B has been identified as a mitochondrial protein with high expression in spermatids. The absence of DNAJC5B induces a cascade of mitochondrial damages, including oxidative stress, mitochondrial stress in the testes, and lower mitochondrial membrane potential of spermatozoa. In vivo and in vitro evidence demonstrates that DNAJC5B mitigates excessive cellular autophagy and mitophagy via DNAJ domain under environmental stress conditions, such as starvation or exposure to mitochondrial uncouplers FCCP and CCCP. This study highlights the important role of DNAJC5B in safeguarding male fertility by preserving mitochondrial function and regulating autophagy during spermiogenesis.
》》部分实验数据展示：
Fig. 6：b Western blot of the LC3B protein in ST cells after amino acids starvation. The LC3B-II significantly decreased in DNAJC5B overexpressing ST cells exposed to starvation and 50 µM autophagy inhibitor chloroquine(CQ).
h, i The relative mRNA expressions of mitochondrial stress-related genes in ST cells treated with DNA JC5B overexpression vectors and 10 µM FCCP (a mitochondrial ROS inducer, h) or 10 µM CCCP (a mitophagy inducer, i) for 6 h. n=4 (plot h) and 3 (plot i), respectively. l The LC3B protein levels in ST cells exposed to 10 µM CCCP for 6 h. m The autophagic flux in ST cells treated with CCCP.
