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Updated: Jan 11, 2026

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Published on: August 4, 2022
Endosomal microautophagy is activated by specific cellular stresses in trout hepatocytes
Emilio J Vélez1,2, Vincent Véron3, Jeanne Gouis3
1INRAE, Université de Pau et des Pays de l'Adour, UMR1419 Nutrition Métabolisme et Aquaculture, 64310, Saint-Pée-sur-Nivelle, France. evelezve@ub.edu.
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, eMI's 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 eMI's 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.
Insights
Endosomal microautophagy (eMI) selectively captures proteins in late endosomes. This study identifies an eMI-like pathway in trout cells, activated by specific cellular stresses, offering new insights into cellular homeostasis and stress responses.
Area of Science:
- Cell Biology
- Molecular Biology
- Autophagy Research
Background:
- Endosomal microautophagy (eMI) is a selective autophagic process.
- eMI captures cytosolic proteins into late endosomes/multivesicular bodies (LE/MVB).
- It shares similarities with chaperone-mediated autophagy (CMA) but utilizes different machinery.
Purpose of the Study:
- To investigate the occurrence and triggers of eMI-like processes in non-mammalian models.
- To understand the stimulus-specific induction of eMI.
- To explore the interplay between eMI and CMA in cellular stress responses.
Main Methods:
- Investigated eMI-like activity in rainbow trout hepatocytes.
- Applied various cellular stress conditions: oxidative stress, high glucose, DNA damage, nutrient deprivation, and serum deprivation.
- Analyzed protein targeting mechanisms involving HSC70, LAMP2A, and ESCRT machinery.
Main Results:
- Identified an eMI-like process in rainbow trout hepatocytes.
- This process was induced by oxidative stress, high glucose, DNA damage, and nutrient deprivation.
- Serum deprivation did not trigger the eMI-like pathway, suggesting stimulus specificity.
- eMI appears to play a compensatory role when CMA is impaired.
Conclusions:
- eMI is a stimulus-specific pathway with a potential role in cellular homeostasis.
- Rainbow trout hepatocytes provide a novel model for studying eMI and its interaction with CMA.
- This research enhances understanding of cellular stress response mechanisms.
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