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Updated: Dec 18, 2025

Dual-color Correlative Light and Electron Microscopy for the Visualization of Interactions between Mitochondria and Lysosomes
Published on: September 27, 2024
MERIT, a cellular system coordinating lysosomal repair, removal and replacement
Jingyue Jia1,2, Aurore Claude-Taupin1,2, Yuexi Gu1,2
1Autophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center , Albuquerque, NM, USA.
The MERIT system, involving galectin 3 (LGALS3), repairs and removes damaged lysosomes. This cellular defense protects endomembrane integrity against various damaging agents.
Area of Science:
- Cell Biology
- Molecular Biology
- Cellular Repair Mechanisms
Background:
- Cellular membrane integrity is crucial for survival and function.
- Existing mechanisms for protecting cellular and intracellular membranes are not fully understood.
- Lysosomal membrane damage can compromise cellular health.
Purpose of the Study:
- To investigate the cellular system MERIT (lysosomal membrane repair, removal, and replacement).
- To elucidate the role of galectins, specifically LGALS3, in lysosomal membrane repair and homeostasis.
- To understand how the MERIT system protects the endolysosomal network.
Main Methods:
- Investigated the MERIT system's sequential steps: ESCRT-dependent repair, autophagy-mediated removal, and lysosomal biogenesis.
- Utilized galectins, particularly LGALS3, as key regulators of the MERIT pathway.
- Examined the interplay between LGALS3, ESCRT components (PDCD6IP/ALIX, CHMP4A, CHMPB), and autophagy receptor TRIM16.
- Assessed the impact of LGALS3 deficiency on lysosomal repair, autophagy, and TFEB-mediated biogenesis.
- Tested the MERIT system's protective capacity against lysosomotropic drugs, Mycobacterium tuberculosis, and MAPT/tau.
Main Results:
- LGALS3 detects lysosomal membrane damage and recruits ESCRT machinery for repair.
- LGALS3 collaborates with TRIM16 to promote the removal of damaged lysosomes via autophagy.
- Absence of LGALS3 impairs repair and autophagy, leading to increased TFEB activation for lysosomal biogenesis.
- The MERIT system effectively protects the endolysosomal network from diverse damaging agents.
Conclusions:
- The MERIT system, governed by LGALS3, is a critical cellular defense mechanism for maintaining lysosomal and endomembrane integrity.
- LGALS3 plays a dual role in initiating lysosomal repair and subsequently engaging autophagy for damaged organelle removal.
- The MERIT pathway provides robust protection against various cellular insults, highlighting its importance in cellular homeostasis.
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