BAIT

CSM3

YMR048W
Replication fork associated factor; required for stable replication fork pausing; component of the DNA replication checkpoint pathway; required for accurate chromosome segregation during meiosis; forms nuclear foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

SIR3

CMT1, MAR2, STE8, chromatin-silencing protein SIR3, L000001896, YLR442C
Silencing protein; interacts with Sir2p, Sir4p, and histone H3 and H4 tails to establish transcriptionally silent chromatin state; required for spreading of silenced chromatin; recruited to chromatin through interaction with Rap1p; C-terminus (residues 840-978) assumes variant winged helix-turn-helix (wH) fold that mediates homodimerization, which is critical for holo-SIR complex loading; SIR3 has a paralog, ORC1, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)

Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

Chromatin determinants impart camptothecin sensitivity.

Puddu F, Salguero I, Herzog M, Geisler NJ, Costanzo V, Jackson SP

Camptothecin-induced locking of topoisomerase 1 on DNA generates a physical barrier to replication fork progression and creates topological stress. By allowing replisome rotation, absence of the Tof1/Csm3 complex promotes the conversion of impending topological stress to DNA catenation and causes camptothecin hypersensitivity. Through synthetic viability screening, we discovered that histone H4 K16 deacetylation drives the sensitivity of yeast cells to ... [more]

EMBO Rep. Jun. 01, 2017; 18(6);1000-1012 [Pubmed: 28389464]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • deletion rescues sensitivity to camptothecin

Curated By

  • BioGRID