The yeast chromatin remodeler Rsc1-RSC complex is required for transcriptional activation of autophagy-related genes and inhibition of the TORC1 pathway in response to nitrogen starvation

The yeast RSC, an ATP-dependent chromatin-remodeling complex, is essential for mitotic and meiotic growth. There are two distinct isoforms of this complex defined by the presence of either Rsc1 or Rsc2; however, the functional differences between these complexes are unclear. Here we show that the RS...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2015-09, Vol.464 (4), p.1248-1253
Main Authors: Yu, Feifei, Imamura, Yuko, Ueno, Masaru, Suzuki, Sho W., Ohsumi, Yoshinori, Yukawa, Masashi, Tsuchiya, Eiko
Format: Article
Language:English
Subjects:
Autophagy - physiology
Autophagy induction
Chromatin remodeling
Chromosomal Proteins, Non-Histone - metabolism
DNA-Binding Proteins - metabolism
Down-Regulation - physiology
Nitrogen - metabolism
RSC
Saccharomyces cerevisiae
Saccharomyces cerevisiae - cytology
Saccharomyces cerevisiae - metabolism
Saccharomyces cerevisiae Proteins - metabolism
Signal Transduction - physiology
TORC1
Transcription Factors - metabolism
Transcriptional Activation - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The yeast RSC, an ATP-dependent chromatin-remodeling complex, is essential for mitotic and meiotic growth. There are two distinct isoforms of this complex defined by the presence of either Rsc1 or Rsc2; however, the functional differences between these complexes are unclear. Here we show that the RSC complex containing Rsc1, but not Rsc2, functions in autophagy induction. Rsc1 was required not only for full expression of ATG8 mRNA but also for maintenance of Atg8 protein stability. Interestingly, decreased autophagic activity and Atg8 protein stability in rsc1Δ cells, but not the defect in ATG8 mRNA expression, were partially suppressed by deletion of TOR1. In addition, we found that rsc1Δ impaired the binding between the Rho GTPase Rho1 and the TORC1-specific component Kog1, which is required for down-regulation of TORC1 activity. These results suggest that the Rsc1-containing RSC complex plays dual roles in the proper induction of autophagy: 1) the transcriptional activation of autophagy-related genes independent of the TORC1 pathway and 2) the inactivation of TORC1, possibly through enhancement of Rho1-Kog1 binding. •The RSC complex containing Rsc1, but not Rsc2, functions in the proper induction of autophagy.•The Rsc1-RSC complex activates transcription of a subset of autophagy-related genes under nitrogen starvation.•Rsc1-RSC is required for proper inactivation of the TORC1 activity through the enhancement of the Rho1-Kog1 interaction.•TORC1 is involved in maintenance of Atg8 protein stability.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2015.07.114