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
Saccharomyces cerevisiae (S288c)
PREY

CDC14

OAF3, phosphoprotein phosphatase CDC14, L000000254, YFR028C
Protein phosphatase required for mitotic exit; required for rDNA segregation, cytokinesis, meiosis I spindle disassembly, and environmental stress response; maintained in nucleolus by Cdc55p in early meiosis until liberated by the FEAR and Mitotic Exit Network in anaphase, enabling it to effect a decrease in CDK/B-cyclin activity and mitotic exit; sequestered in metaphase II, then released again upon entry into anaphase II
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Publication

The RSC chromatin-remodeling complex influences mitotic exit and adaptation to the spindle assembly checkpoint by controlling the Cdc14 phosphatase.

Rossio V, Galati E, Ferrari M, Pellicioli A, Sutani T, Shirahige K, Lucchini G, Piatti S

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: resistance to chemicals (APO:0000087)
  • phenotype: cell cycle progression (APO:0000253)

Additional Notes

  • genetic complex
  • overexpression of a dominant variant of CDC14, cdc14TAB6-1, restores the ability of nocodazole treated mad2/rsc2 mutant cells to rereplicate DNA

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RSC2 CDC14
Synthetic Lethality
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.

Low-BioGRID
502357

Curated By

  • BioGRID