ArticleMolecular and cellular biology2005
The Ccr4-Not complex independently controls both Msn2-dependent transcriptional activation--via a newly identified Glc7/Bud14 type I protein phosphatase module--and TFIID promoter distribution.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 72 citations in OpenAlex.
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- Regulated resource reallocation is transcriptionally hard wired into the yeast stress response.bioRxiv : the preprint server for biology · 2024Article
- Glycogen synthase activity inmSphere · 2024Article
- Disruption of the Mammalian Ccr4-Not Complex Contributes to Transcription-Mediated Genome Instability.Cells · 2023Article
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- The C-terminal region of yeast ubiquitin-protein ligase Not4 mediates its cellular localization and stress response.FEMS microbiology letters · 2021Article
- Review
- Improvement in D-xylose utilization and isobutanol production in S. cerevisiae by adaptive laboratory evolution and rational engineering.Journal of industrial microbiology & biotechnology · 2020Article
- Mitochondria-cytosol-nucleus crosstalk: learning from Saccharomyces cerevisiae.FEMS yeast research · 2018Review
- A constitutive active allele of the transcription factor Msn2 mimicking low PKA activity dictates metabolic remodeling in yeast.Molecular biology of the cell · 2018Article
- Article
- The Candida albicans transcription factor Cas5 couples stress responses, drug resistance and cell cycle regulation.Nature communications · 2017Article
- Cytoplasmic deadenylase Ccr4 is required for translational repression of LRG1 mRNA in the stationary phase.PloS one · 2017Article
- The Ccr4-Not complex is a key regulator of eukaryotic gene expression.Wiley interdisciplinary reviews. RNA · 2016Review
- Identification of novel small ncRNAs in pollen of tomato.BMC genomics · 2015Article
- Expression of three topologically distinct membrane proteins elicits unique stress response pathways in the yeast Saccharomyces cerevisiae.Physiological genomics · 2015Article
- The Not5 subunit of the ccr4-not complex connects transcription and translation.PLoS genetics · 2014Article
- Saccharomyces cerevisiae genes involved in survival of heat shock.G3 (Bethesda, Md.) · 2013Article
- Transcriptome analysis of Anopheles stephensi embryo using expressed sequence tags.Journal of biosciences · 2013Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ccr4-Not complex is a conserved global regulator of gene expression, which serves as a regulatory platform that senses and/or transmits nutrient and stress signals to various downstream effectors. Presumed effectors of this complex in yeast are TFIID, a general transcription factor that associates with the core promoter, and Msn2, a key transcription factor that regulates expression of stress-responsive element (STRE)-controlled genes. Here we show that the constitutively high level of STRE-driven expression in ccr4-not mutants results from two independent effects. Accordingly, loss of Ccr4-Not function causes a dramatic Msn2-independent redistribution of TFIID on promoters with a particular bias for STRE-controlled over ribosomal protein gene promoters. In parallel, loss of Ccr4-Not complex function results in an alteration of the posttranslational modification status of Msn2, which depends on the type 1 protein phosphatase Glc7 and its newly identified subunit Bud14. Tests of epistasis as well as transcriptional analyses of Bud14-dependent transcription support a model in which the Ccr4-Not complex prevents activation of Msn2 via inhibition of the Bud14/Glc7 module in exponentially growing cells. Thus, increased activity of STRE genes in ccr4-not mutants may result from both altered general distribution of TFIID and unscheduled activation of Msn2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.