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 endosome- and lysosome-associated RAB-7 is reduced in mutants， and this defect is rescued by simultaneous loss of function of Expression of the GDP-bound form of RAB-7 also promotes lysosomal biogenesis and suppresses the autophagy defect in mutants. Our study reveals that the RBG-1-RBG-2 complex acts by modulating the dynamics of membrane-associated RAB-7 to regulate lysosomal biogenesis， and provides insights into the pathogenesis of Vici syndrome.