| Literature DB >> 26986811 |
Chao Liu1,2, Hongna Wang1,2, Yongliang Shang1,2, Weixiao Liu1, Zhenhua Song1,2, Haichao Zhao1,2, Lina Wang1,2, Pengfei Jia3, Fengyi Gao1, Zhiliang Xu1,2, Lin Yang3, Fei Gao1,2, Wei Li1,2.
Abstract
The ectoplasmic specialization (ES) is essential for Sertoli-germ cell communication to support all phases of germ cell development and maturity. Its formation and remodeling requires rapid reorganization of the cytoskeleton. However, the molecular mechanism underlying the regulation of ES assembly is still largely unknown. Here, we show that Sertoli cell-specific disruption of autophagy influenced male mouse fertility due to the resulting disorganized seminiferous tubules and spermatozoa with malformed heads. In autophagy-deficient mouse testes, cytoskeleton structures were disordered and ES assembly was disrupted. The disorganization of the cytoskeleton structures might be caused by the accumulation of a negative cytoskeleton organization regulator, PDLIM1, and these defects could be partially rescued by Pdlim1 knockdown in autophagy-deficient Sertoli cells. Altogether, our works reveal that the degradation of PDLIM1 by autophagy in Sertoli cells is important for the proper assembly of the ES, and these findings define a novel role for autophagy in Sertoli cell-germ cell communication.Entities:
Keywords: Atg5; Atg7; PDLIM1; autophagy; cytoskeleton organization; ectoplasmic specialization
Mesh:
Year: 2016 PMID: 26986811 PMCID: PMC4854559 DOI: 10.1080/15548627.2016.1159377
Source DB: PubMed Journal: Autophagy ISSN: 1554-8627 Impact factor: 16.016