Target of rapamycin signaling mediates vacuolar fission caused by endoplasmic reticulum stress in Saccharomyces cerevisiae.

ABSTRACT: The yeast vacuole is equivalent to the mammalian lysosome and, in response to diverse physiological and environmental stimuli, undergoes alterations both in size and number. Here we demonstrate that vacuoles fragment in response to stress within the endoplasmic reticulum (ER) caused by chemical or genetic perturbations. We establish that this response does not involve known signaling pathways linked previously to ER stress but instead requires the rapamycin-sensitive TOR Complex 1 (TORC1), a master regulator of cell growth, together with its downstream effectors, Tap42/Sit4 and Sch9. To identify additional factors required for ER stress-induced vacuolar fragmentation, we conducted a high-throughput, genome-wide visual screen for yeast mutants that are refractory to ER stress-induced change

SUBMITTER: Stauffer B 

PROVIDER: S-EPMC4678019 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature