BAIT
RSC2
L000004025, YLR357W
Component of the RSC chromatin remodeling complex; required for expression of mid-late sporulation-specific genes; involved in telomere maintenance; RSC2 has a paralog, RSC1, that arose from the whole genome duplication
GO Process (9)
GO Function (1)
GO Component (1)
Gene Ontology Biological Process
- ATP-dependent chromatin remodeling [IDA]
- UV-damage excision repair [IMP]
- chromosome segregation [IGI]
- double-strand break repair via homologous recombination [IMP]
- double-strand break repair via nonhomologous end joining [IPI]
- nucleosome disassembly [IDA]
- plasmid maintenance [IMP]
- sister chromatid cohesion [IMP]
- transcription elongation from RNA polymerase II promoter [IDA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
PREY
DBF2
serine/threonine-protein kinase DBF2, L000000487, YGR092W
Ser/Thr kinase involved in transcription and stress response; functions as part of a network of genes in exit from mitosis; localization is cell cycle regulated; activated by Cdc15p during the exit from mitosis; also plays a role in regulating the stability of SWI5 and CLB2 mRNAs; phosphorylates Chs2p to regulate primary septum formation and Hof1p to regulate cytokinesis; DBF2 has a paralog, DBF20, that arose from the whole genome duplication
GO Process (5)
GO Function (3)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
The RSC chromatin-remodeling complex influences mitotic exit and adaptation to the spindle assembly checkpoint by controlling the Cdc14 phosphatase.
Upon prolonged activation of the spindle assembly checkpoint, cells escape from mitosis through a mechanism called adaptation or mitotic slippage, which is thought to underlie the resistance of cancer cells to antimitotic drugs. We show that, in budding yeast, this mechanism depends on known essential and nonessential regulators of mitotic exit, such as the Cdc14 early anaphase release (FEAR) pathway ... [more]
J. Cell Biol. Nov. 29, 2010; 191(5);981-97 [Pubmed: 21098112]
Throughput
- Low Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
- phenotype: heat sensitivity (APO:0000147)
Curated By
- BioGRID