High levels of autophagy exist in Leydig cells of the testis, but its physiological function is unknown. Gao et al. now show that autophagy promotes uptake of cholesterol, an essential precursor for testosterone synthesis, by removing the NHERF2 negative regulator of the high-density lipoprotein receptor SR-BI.

The aim of present work was to investigate the effect of solid-state fermentation with filamentous fungi (Aspergillus oryzae var. effuses, Aspergillus oryzae, and Aspergillus niger) on total phenolics content (TPC), flavonoids, and antioxidant activities of four subfractions of oat, namely, n-hexane, ethyl acetate (EA), n-butanol, and water, and compare them to their corresponding subfractions of unfermented oat. The TPC and total flavonoids increased dramatically, especially in EA subfractions (p < 0.05). The levels of antioxidant activity of subfractions were also significantly enhanced (p < 0.05). The highest antioxidant activities were also found in the EA subfractions. The polyphenols in EA were analyzed by high-performance liquid chromatography at 280 nm. Most polyphenols were increased remarkably, especially ferulic and caffeic acids. There was a clear correlation between the TPC and antioxidant activity. In conclusion, fungi fermentation is a potential bioprocess for increasing the TPC, flavonoids, and antioxidant activities of oat-based food.

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.