Endosomal Microautophagy is Activated by Specific Cellular Stresses in Trout Hepatocytes

Abstract

Endosomal microautophagy (eMI) is a recently discovered autophagic process where cytosolic proteins are selectively captured in late endosome/multivesicular bodies (LE/MVB). This pathway, similar to chaperone-mediated autophagy (CMA), involves the recognition of KFERQ-like motif containing proteins by HSC70. While CMA targets substrates to lysosomes via the receptor LAMP2A, eMI involves internalization into intraluminal vesicles within LE/MVB through interactions with ESCRT machinery. Although the same proteins could be targeted by either pathway, eMIs role in cellular homeostasis is less understood. Our research identified an eMI-like process in rainbow trout hepatocytes, triggered by oxidative stress, high-glucose, DNA damage, and nutrient deprivation, but not serum deprivation. This finding suggests eMIs stimulus-specific induction and its potential compensatory role when CMA is impaired. Our study provides new insights into eMI and offers novel model organisms for exploring its interactions with CMA, enhancing our understanding of cellular stress responses.