Activation of the RAS/cyclic AMP pathway suppresses a TOR deficiency in yeast
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 153770
Author(s) Schmelzle, T.; Beck, T.; Martin, D. E.; Hall, M. N.
Author(s) at UniBasel Hall, Michael N.
Year 2004
Title Activation of the RAS/cyclic AMP pathway suppresses a TOR deficiency in yeast
Journal Molecular and Cellular Biology
Volume 24
Number 1
Pages / Article-Number 338-351
Keywords 1-Phosphatidylinositol 3-Kinase/deficiency/*metabolism; Antifungal Agents/pharmacology; Autophagy/drug effects; Cell Cycle Proteins; Cyclic AMP/*metabolism; DNA-Binding Proteins/metabolism; *Fungal Proteins; Glycogen/metabolism; Monosaccharide Transport Proteins/drug effects; Phosphotransferases (Alcohol Group Acceptor)/deficiency/*metabolism; Ribosomes/drug effects; Saccharomyces cerevisiae/metabolism; Saccharomyces cerevisiae Proteins/*metabolism; Sirolimus/pharmacology; Transcription Factors/metabolism; Transcription; Genetic; ras Proteins/drug effects/*metabolism
Abstract

The TOR (target of rapamycin) and RAS/cyclic AMP (cAMP) signaling pathways are the two major pathways controlling cell growth in response to nutrients in yeast. In this study we examine the functional interaction between TOR and the RAS/cAMP pathway. First, activation of the RAS/cAMP signaling pathway confers pronounced resistance to rapamycin. Second, constitutive activation of the RAS/cAMP pathway prevents several rapamycin-induced responses, such as the nuclear translocation of the transcription factor MSN2 and induction of stress genes, the accumulation of glycogen, the induction of autophagy, the down-regulation of ribosome biogenesis (ribosomal protein gene transcription and RNA polymerase I and III activity), and the down-regulation of the glucose transporter HXT1. Third, many of these TOR-mediated responses are independent of the previously described TOR effectors TAP42 and the type 2A-related protein phosphatase SIT4. Conversely, TOR-controlled TAP42/SIT4-dependent events are not affected by the RAS/cAMP pathway. Finally, and importantly, TOR controls the subcellular localization of both the protein kinase A catalytic subunit TPK1 and the RAS/cAMP signaling-related kinase YAK1. Our findings suggest that TOR signals through the RAS/cAMP pathway, independently of TAP42/SIT4. Therefore, the RAS/cAMP pathway may be a novel TOR effector branch.

Publisher American Society for Microbiology
ISSN/ISBN 1098-5549
edoc-URL http://edoc.unibas.ch/dok/A5258152
Full Text on edoc No
Digital Object Identifier DOI 10.1128/MCB.24.1.338-351.2004
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/14673167
ISI-Number WOS:000187531200030
Document type (ISI) Journal Article
 
   

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