Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA173726 | ENA |
REPOSITORIES: ENA
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Project description:DNA damage results in the activation of checkpoint kinases, which phosphorylate downstream effectors that inhibit the cell cycle, activate DNA repair, and cause widespread changes in transcription. However, the specific connections between the checkpoint kinases and downstream transcription factors (TFs) are not well understood. Here, we introduce a strategy for mapping regulatory networks between kinases and TFs involving integration of kinase mutant expression profiles, transcriptional regulatory interactions, and phosphoproteomics. We use this approach to investigate the role of the Saccharomyces cerevisiae checkpoint kinases (Mec1, Tel1, Chk1, Rad53, and Dun1) in the transcriptional response to DNA damage caused by methyl methanesulfonate (MMS). The result is a global kinase-TF regulatory network in which Mec1 and Tel1 signal through Rad53 to synergistically regulate the expression of more than 600 genes. This network implicates at least nine TFs, including Msn4, Gcn4, SBF (Swi4/Swi6), MBF (Swi6/Mbp1), and Fkh2/Ndd1/Mcm1, nearly all of which have sites of Rad53-dependent phosphorylation, as downstream regulators of checkpoint kinase-dependent genes. We also identify a major DNA damage-induced transcriptional network acting independently of Rad53 and other checkpoint kinases to regulate expression of genes involved in general and oxidative stress responses. Expression was profiled with and without MMS treatment in several genetic backgrounds (gene deletion strains).
2013-03-31 | E-GEOD-40351 | biostudies-arrayexpress
Project description:DNA damage results in the activation of checkpoint kinases, which phosphorylate downstream effectors that inhibit the cell cycle, activate DNA repair, and cause widespread changes in transcription. However, the specific connections between the checkpoint kinases and downstream transcription factors (TFs) are not well understood. Here, we introduce a strategy for mapping regulatory networks between kinases and TFs involving integration of kinase mutant expression profiles, transcriptional regulatory interactions, and phosphoproteomics. We use this approach to investigate the role of the Saccharomyces cerevisiae checkpoint kinases (Mec1, Tel1, Chk1, Rad53, and Dun1) in the transcriptional response to DNA damage caused by methyl methanesulfonate (MMS). The result is a global kinase-TF regulatory network in which Mec1 and Tel1 signal through Rad53 to synergistically regulate the expression of more than 600 genes. This network implicates at least nine TFs, including Msn4, Gcn4, SBF (Swi4/Swi6), MBF (Swi6/Mbp1), and Fkh2/Ndd1/Mcm1, nearly all of which have sites of Rad53-dependent phosphorylation, as downstream regulators of checkpoint kinase-dependent genes. We also identify a major DNA damage-induced transcriptional network acting independently of Rad53 and other checkpoint kinases to regulate expression of genes involved in general and oxidative stress responses.
2013-03-31 | GSE40351 | GEO
Project description:A network governing DNA integrity was identified in yeast by a global genetic analysis of synthetic fitness or lethality defect (SFL) interactions. Within this network, multiple functional modules or mini-pathways were defined according to their common patterns of global SFL interactions and available protein-protein interaction information. Modules or genes involved in DNA replication, DNA replication checkpoint signaling, and oxidative stress response were identified as the major guardians against lethal spontaneous DNA damage, efficient repair of which requires the functions of the DNA damage checkpoint signaling and multiple DNA repair pathways. This genome-wide genetic interaction network also revealed potential roles of a number of genes and modules in mitotic DNA replication and maintenance of genomic stability. These include DIA2, NPT1, HST3, HST4, and the CSM1/LRS4 module (CSM1m). Likewise, the CTF18 module (CTF18m), previously implicated in sister chromatid cohesion, was found to participate in the DNA replication checkpoint. Keywords: dose response
2006-02-16 | GSE3574 | GEO
Project description:RNA-dependent chromatin association of transcription elongation factors and Pol II CTD kinases
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Project description:Cyclin-dependent kinases are regulators and effectors of oscillations driven by a transcription factor network
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Project description:Environment-responsive transcription factors bind proto-silencer elements and regulate subtelomeric silencing
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Project description:Global Control of cell cycle transcription by coupled CDK and network oscillators
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Project description:In Saccharomyces cerevisiae, the kinase Rio1 regulates rDNA transcription and segregation, pre-rRNA cleavage, and 40S ribosomal subunit maturation. Other roles are unknown. Human orthologue RIOK1; which is frequently overexpressed in malignancies, drives tumor growth and metastasis. Again, also RIOK1 biology is poorly understood. In this study, we charted the global activity of Rio1 in budding yeast. By producing and systems-integrating its protein-interaction, gene-transcription, and chromatin-binding maps we generated Rio1's multi-layered activity network, which controls protein synthesis and turnover, metabolism, growth, proliferation, and genetic stability. Rio1 regulates itself at the transcriptional level, and manages its network both directly and indirectly, via a battery of regulators and transcription factors, including Gcn4. We experimentally confirmed the network and show that Rio1 commands its downstream circuit depending on the growth conditions encountered. We also find that Rio1 and RIOK1 activities are functionally equivalent. Our data suggest that pathological RIOK1 expression may deregulate its network and fuel promiscuous transcription and ribosome production, uncontrolled metabolism, growth, proliferation, and chromosomal instability; well-known contributors to cancer initiation, maintenance and metastasis.
2020-11-23 | GSE107318 | GEO
Project description:Gcn2p regulates a G1/S cell cycle checkpoint in response to DNA damage
| PRJNA100979 | ENA
Project description:Inhibitors of checkpoint kinase 1 (CHK1),a central component of DNA damage and cell cycle checkpoint response, represent a promising new cancer therapy, but the global cellular functionsthey regulate through phosphorylationare poorly understood. To elucidate the CHK1-regulated phosphorylation network, we performed a global quantitative phosphoproteomics analysis, which revealed 142 phosphositeswhose phosphorylation levels were significantly different following treatment with the CHK1 inhibitor SCH 900776.
2020-04-23 | PXD015125 | Pride