Saccharomyces cerevisiae Ras/cAMP pathway controls post-diauxic shift element-dependent transcription through the zinc finger protein Gis1

Autor: Claudio De Virgilio, Niels Bürckert, Ivo Pedruzzi, Pascal Egger
Rok vydání: 2000
Předmět:
Saccharomyces cerevisiae Proteins
Transcription
Genetic
Recombinant Fusion Proteins
Saccharomyces cerevisiae
Gene Dosage
Cell Cycle Proteins
Biology
Second Messenger Systems
General Biochemistry
Genetics and Molecular Biology
Fungal Proteins
Bacterial Proteins
Genes
Reporter
Gene Expression Regulation
Fungal
Cyclic AMP
HSP70 Heat-Shock Proteins
Phosphorylation
DNA
Fungal
Protein kinase A
Molecular Biology
Heat-Shock Proteins
Derepression
Histone Demethylases
Regulation of gene expression
Zinc finger
Fungal protein
Binding Sites
General Immunology and Microbiology
General Neuroscience
Serine Endopeptidases
Fungal genetics
Epistasis
Genetic
Zinc Fingers
Articles
biology.organism_classification
Cyclic AMP-Dependent Protein Kinases
Molecular biology
Culture Media
Repressor Proteins
ras Proteins
cAMP-dependent pathway
Protein Kinases
Protein Processing
Post-Translational
Cell Division
Zdroj: Scopus-Elsevier
ISSN: 1460-2075
Popis: The Saccharomyces cerevisiae protein kinase Rim15 was identified previously as a component of the Ras/cAMP pathway acting immediately downstream of cAMP-dependent protein kinase (cAPK) to control a broad range of adaptations in response to nutrient limitation. Here, we show that the zinc finger protein Gis1 acts as a dosage-dependent suppressor of the rim15Delta defect in nutrient limitation-induced transcriptional derepression of SSA3. Loss of Gis1 results in a defect in transcriptional derepression upon nutrient limitation of various genes that are negatively regulated by the Ras/cAMP pathway (e.g. SSA3, HSP12 and HSP26). Tests of epistasis as well as transcriptional analyses of Gis1-dependent expression indicate that Gis1 acts in this pathway downstream of Rim15 to mediate transcription from the previously identified post-diauxic shift (PDS) element. Accordingly, deletion of GIS1 partially suppresses, and overexpression of GIS1 exacerbates the growth defect of mutant cells that are compromised for cAPK activity. Moreover, PDS element-driven expression, which is negatively regulated by the Ras/cAMP pathway and which is induced upon nutrient limitation, is almost entirely dependent on the presence of Gis1.
Databáze: OpenAIRE
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