STY1
Gene Ontology Biological Process
- G1 cell cycle arrest in response to nitrogen starvation [IMP]
- G1 to G0 transition [IMP]
- MAPK cascade in response to starvation [IMP]
- MAPK cascade involved in osmosensory signaling pathway [IDA, IMP]
- cellular response to cation stress [IGI]
- cellular response to nitrogen starvation [IMP]
- mRNA export from nucleus in response to heat stress [IMP]
- mitotic cell cycle arrest in response to nitrogen starvation [IMP]
- positive regulation of G2/M transition of mitotic cell cycle [IMP]
- positive regulation of transcription factor import into nucleus in response to oxidative stress [IMP]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- positive regulation of transcription from RNA polymerase II promoter in response to oxidative stress [IMP]
- regulation of DNA binding [IDA]
- regulation of cAMP-mediated signaling [IMP]
- regulation of cAMP-mediated signaling by regulation of transcription from RNA polymerase II promoter [IMP]
- regulation of cell shape involved in G1 to G0 transition [IMP]
- regulation of chromatin assembly [IMP]
- regulation of chromatin disassembly [IMP]
- regulation of histone acetylation [IMP]
- regulation of mRNA stability involved in cellular response to UV [IMP]
- regulation of meiotic cell cycle [IMP]
- regulation of reciprocal meiotic recombination [IMP]
- regulation of translation in response to nitrogen starvation [IDA]
- regulation of translation in response to osmotic stress [IDA, IMP]
- regulation of translation in response to oxidative stress [IDA, IMP]
- stress granule assembly [IMP]
- stress granule disassembly [IMP]
- stress-activated MAPK cascade [IMP]
Gene Ontology Molecular Function
CLP1
Gene Ontology Biological Process
- cellular response to DNA damage stimulus [IMP]
- chromosome passenger complex localization to spindle midzone [IMP]
- cytokinesis after mitosis checkpoint [IMP]
- cytokinesis checkpoint [IGI]
- mitotic actomyosin contractile ring maintenance [IGI, IMP]
- negative regulation of G2/M transition of mitotic cell cycle [IMP]
- negative regulation of cyclin-dependent protein serine/threonine kinase activity [IGI]
- negative regulation of protein kinase activity [IMP]
- positive regulation of attachment of spindle microtubules to kinetochore involved in mitotic sister chromatid segregation [IMP]
- positive regulation of septation initiation signaling [IGI]
- regulation of exit from mitosis [IMP]
- regulation of mitotic sister chromatid segregation [IMP]
- response to mitotic cell cycle spindle assembly checkpoint signaling [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Phenotypic Enhancement
A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.
Publication
A systematic screen reveals new elements acting at the G2/M cell cycle control.
ABSTRACT: BACKGROUND: The major cell cycle control acting at the G2 to mitosis transition is triggered in all eukaryotes by cyclin-dependent kinases (CDKs). In the fission yeast Schizosaccharomyces pombe the activation of the G2/M CDK is regulated primarily by dephosphorylation of the conserved residue Tyr15 in response to the stress-nutritional response and cell geometry sensing pathways. To obtain a more ... [more]
Throughput
- Low Throughput
Ontology Terms
- phenotype: cell size (APO:0000052)
Additional Notes
- double mutants show decreased cell length at the time of division
Related interactions
Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
---|---|---|---|---|---|---|
STY1 CLP1 | Negative Genetic Negative Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores. | High | -4.6324 | BioGRID | 759667 |
Curated By
- BioGRID