Glucose regulates clathrin adaptors at thetrans-Golgi network and endosomes

• DOI: 10.1091/mbc.e11-04-0309
• Publication Date: 2011-08-11T03:48:22Z
• Authors: Quyen L. Aoh; Lee M. Graves; Mara C. Duncan
• Keywords: Snf3

Glucose is a rich source of energy and the raw material for biomass increase. Many eukaryotic cells remodel their physiology in presence absence glucose. The yeast Saccharomyces cerevisiae undergoes changes transcription, translation, metabolism, cell polarity response to glucose availability. Upon starvation, translation initiation are immediately inhibited, then gradually recover. In this paper, we provide evidence that, as traffic at trans-Golgi network (TGN) endosomes regulated by via an unknown mechanism that depends on protein kinase A (PKA). withdrawal, clathrin adaptors exhibit biphasic change localization: they initially delocalize from membrane within minutes later partially recover onto membranes. Additionally, removal induces posttranslational modifications adaptors. Ras Gpr1 signaling pathways, which converge PKA, required adaptor localization modifications. Acute inhibition PKA demonstrates prior withdrawal prevents several responses starvation. This study activity starvation primes TGN