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The RBG-1-RBG-2 complex modulates autophagy activity by regulating lysosomal biogenesis and function in C. elegans.

J Cell Sci. 2019; 
Wang Zhaoyu,Zhao Hongyu,Yuan Chongzhen,Zhao Dongfeng,Sun Yanan,Wang Xiaochen,Zhang
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Catalog Antibody The samples were subjected to SDS-PAGE and signals were detected with diluted polyclonal rat anti-RAB-7 (Chen et al., 2010) and monoclonal mouse anti-Trx-tag (Genscript, A00180-40) primary antibodies (diluted 1:1000, unless specifically indicated) and peroxidase AffiniPure goat anti-rat IgG (Jackson ImmunoResearch, 112-035-003), HRP-goat anti-mouse (Jackson ImmunoResearch, 115-035-003) secondary antibodies (diluted 1:200). Get A Quote

摘要

Vici syndrome is a severe and progressive multisystem disease caused by mutations in the gene. In patient tissues and animal models, loss of function is associated with defective autophagy caused by accumulation of non-degradative autolysosomes, but very little is known about the mechanism underlying this cellular phenotype. Here, we demonstrate that loss of function of the RBG-1-RBG-2 complex ameliorates the autophagy defect in mutants. The suppression effect is independent of the complex's activity as a RAB-3 GAP and a RAB-18 GEF. Loss of activity promotes lysosomal biogenesis and function, and also suppresses the accumulation of non-functional autolysosomes in mutants. The mobility of late endos... More

关键词

Autophagy,C. elegans,Lysosome,RAB-7,RAB3GAP1,RBG-1,e