Collapse of late endosomal pH elicits a rapid Rab7 response via V-ATPase and RILP.

Using a lysosomal damage model, Mulligan et al. demonstrates that pH collapse in otherwise undamaged late endosomes leads to V-ATPase- and RILP-mediated hyperactivation of the small GTPase Rab7, disrupting normal late endosome tubulation behavior and biosynthetic receptor trafficking. These findings suggest a pH driven late endosomal stress response.