Galectins and TRIMs directly interact and orchestrate autophagic response to endomembrane damage.
Autophagy
; 13(6): 1086-1087, 2017 Jun 03.
Article
en En
| MEDLINE
| ID: mdl-28368693
ABSTRACT
Macroautophagy/autophagy is a homeostatic process delivering cytoplasmic targets, including damaged organelles, to lysosomes for degradation; however, it is not completely understood how compromised endomembranes are recognized by the autophagic apparatus. We have described previously that the TRIM family of proteins act as receptors for selective autophagy. In this study we uncovered the property of TRIMs to directly interact with members of the family of cytosolic lectins termed galectins. Galectins patrol the cytoplasm and recognize compromised membranes. We show that TRIM16 uses LGALS3 (galectin 3) to detect damaged lysosomes and phagosomes. TRIM16 assembles the core autophagic machinery and is found in protein complexes with MTOR and TFEB, thus regulating their activity to set in motion endomembrane quality control. The TRIM16-LGALS3 system plays a key role in autophagic homeostasis of lysosomes and in the control of Mycobacterium tuberculosis in vivo.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
3_ND
Problema de salud:
3_tuberculosis
Asunto principal:
Endosomas
/
Autofagia
/
Galectinas
/
Proteínas de Motivos Tripartitos
/
Membranas Intracelulares
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Autophagy
Año:
2017
Tipo del documento:
Article
País de afiliación:
Estados Unidos