Trs130 Participates in Autophagy Through GTPases Ypt31/32 in Saccharomyces cerevisiae. (21st November 2012)

• Record Type: Journal Article
• Authors: Zou, Shenshen; Chen, Yong; Liu, Yutao; Segev, Nava; Yu, Sidney; Liu, Yan; Min, Gaoyi; Ye, Min; Zeng, Yan; Zhu, Xiaoping; Hong, Bing; Björn, Lars Olof; Liang, Yongheng; Li, Shaoshan; Xie, Zhiping
• Is Part Of: Traffic. Volume 14:Number 2(2013:Feb.)
• Page Start: 233
• Page End: 246
• Publication Date: 2012-11-21
• Subjects: Biological transport -- Periodicals; 571.6
• DOI: 10.1111/tra.12024
• Languages: English
• ISSNs: 1398-9219

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p> <bold>Trs130 is a specific component of the transport protein particle II complex, which functions as a guanine nucleotide exchange factor (GEF) for Rab GTPases Ypt31/32. Ypt31/32 is known to be involved in autophagy, although the precise mechanism has not been thoroughly studied. In this study, we investigated the potential involvement of Trs130 in autophagy and found that both the cytoplasm‐to‐vacuole targeting (Cvt) pathway and starvation‐induced autophagy were defective in a <italic>trs130ts</italic> (<italic>trs130</italic> temperature‐sensitive) mutant. Mutant cells could not transport Atg8 and Atg9 to the pre‐autophagosomal structure/phagophore assembly site (PAS) properly, resulting in multiple Atg8 dots and Atg9 dots dispersed in the cytoplasm. Some dots were trapped in the trans‐Golgi. Genetic studies showed that the effect of the Trs130 mutation was downstream of Atg5 and upstream of Atg1, Atg13, Atg9 and Atg14 on the autophagic pathway. Furthermore, overexpression of Ypt31 or Ypt32, but not of Ypt1, rescued autophagy defects in <italic>trs130ts</italic> and <italic>trs65ts</italic> (<italic>Trs130‐HA Trs120‐myc trs65Δ</italic>) mutants. Our data provide mechanistic insight into how Trs130 participates in autophagy and suggest that vesicular trafficking regulated by GTPases/GEFs is important in the transport of autophagy proteins from the trans‐Golgi to the PAS.</bold> </p> </abstract>