Autophagy and Cathepsin D mediated apoptosis contributing to ovarian follicular atresia in the Nile tilapia.

Abstract

Follicular atresia is a hormonally controlled degenerative process involving apoptosis of the somatic and germ cells. Since different signaling pathways can induce cell death, the aim of the present study was to investigate cell death signaling and crosstalk between autophagic, apoptotic, and lysosomal proteins during follicular atresia in Nile tilapia. For this, females were kept in controlled conditions for 21 days, and ovary samples were collected weekly. The atretic follicles (AF) were analyzed in three regression phases: Early, advanced, and late. Under electron microscopy, the follicular cells exhibited numerous protein synthesis organelles in the early AF. Immunoreactivity for Bcl2, Beclin1, Lc3, and Cathepsin D increased significantly in advanced AF (p < .001), when follicular cells were in intense yolk phagocytosis. In this phase, autophagosomes and autolysosomes were frequently observed. In the late AF, follicular cells had a markedly electron-lucid cytoplasm and immunoreactivity for Bax and TUNEL assay indicated an elevated apoptosis rate. Colocalisation of Lamp1/Cathepsin D and Lc3/Caspase-3 suggests dynamic crosstalk between the autophagy, apoptosis, and lysosome pathways. Taken together, the data indicate that autophagy plays a role in the homeostasis and clearance of the follicular cells preceding Cathepsin D mediated apoptosis during follicular atresia in Nile tilapia.