ArticleThe Journal of biological chemistry2002
Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.
Article in The Journal of biological chemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Rapamycin-sensitive mechanisms confine the growth of fission yeast below the temperatures detrimental to cell physiology.iScience · 2024Article
- Mitochondrial Retrograde Signaling Contributes to Metabolic Differentiation in Yeast Colonies.International journal of molecular sciences · 2021Article
- N- and C-terminal Gln3-Tor1 interaction sites: one acting negatively and the other positively to regulate nuclear Gln3 localization.Genetics · 2021Article
- The secret messages between mitochondria and nucleus in muscle cell biology.Archives of biochemistry and biophysics · 2019Review
- Metabolic profiling of retrograde pathway transcription factors rtg1 and rtg3 knockout yeast.Metabolites · 2014Article
- Article
- The retrograde response: when mitochondrial quality control is not enough.Biochimica et biophysica acta · 2013Review
- Yeast as a tool to study signaling pathways in mitochondrial stress response and cytoprotection.TheScientificWorldJournal · 2012Review
- Nitrogen-responsive regulation of GATA protein family activators Gln3 and Gat1 occurs by two distinct pathways, one inhibited by rapamycin and the other by methionine sulfoximine.The Journal of biological chemistry · 2011Article
- Transcriptional regulation in yeast during diauxic shift and stationary phase.Omics : a journal of integrative biology · 2010Review
- Distinct phosphatase requirements and GATA factor responses to nitrogen catabolite repression and rapamycin treatment in Saccharomyces cerevisiae.The Journal of biological chemistry · 2010Article
- Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae.Current genetics · 2010Review
- Glucose signaling-mediated coordination of cell growth and cell cycle in Saccharomyces cerevisiae.Sensors (Basel, Switzerland) · 2010Review
- A genome-wide screen for regulators of TORC1 in response to amino acid starvation reveals a conserved Npr2/3 complex.PLoS genetics · 2009Article
- Article
- Rapamycin-induced Gln3 dephosphorylation is insufficient for nuclear localization: Sit4 and PP2A phosphatases are regulated and function differently.The Journal of biological chemistry · 2009Article
- Formalin can alter the intracellular localization of some transcription factors in Saccharomyces cerevisiae.FEMS yeast research · 2008Article
- Tor pathway control of the nitrogen-responsive DAL5 gene bifurcates at the level of Gln3 and Gat1 regulation in Saccharomyces cerevisiae.The Journal of biological chemistry · 2008Article
- Hsf1 activation inhibits rapamycin resistance and TOR signaling in yeast revealed by combined proteomic and genetic analysis.PloS one · 2008Article
- Yeast aconitase binds and provides metabolically coupled protection to mitochondrial DNA.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively. The accepted pathway for this regulation is NH(3) or excess nitrogen dash, vertical Mks1p dash, vertical Ure2p dash, vertical Gln3p --> DAL5, and rapamycin or limiting nitrogen dash, vertical Torp --> Tap42 dash, vertical Mks1p --> Rtg1/3p --> CIT2, respectively. In current models, Mks1p positively regulates both Gln3p (and DAL5 expression) and Rtg1/3p (and CIT2 expression). Here, in contrast, we show the following. (i) Mks1p is a strong negative regulator of CIT2 expression and does not effect NCR-sensitive expression of DAL5 or GAP1. (ii) Retrograde carbon and NCR-sensitive nitrogen metabolism are not linked by the quality of the nitrogen source, i.e. its ability to elicit NCR, but by the product of its catabolism, i.e. glutamate or ammonia. (iii) In some instances, we can dissociate rapamycin-induced CIT2 expression from Mks1p function, i.e. rapamycin does not suppress Mks1p-mediated down-regulation of CIT2 expression. These findings suggest that currently accepted models of Tor1/2p signal transduction pathway regulation require revision.
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