BAIT

DPB11

protein kinase activating protein DPB11, L000003001, YJL090C
DNA replication initiation protein; loads DNA pol epsilon onto pre-replication complexes at origins; checkpoint sensor recruited to stalled replication forks by the checkpoint clamp complex where it activates Mec1p; along with Rfa1p, binds to ultrafine anaphase bridges in mitotic cells and prevents accumulation of chromatin bridges by stimulating the Mec1p kinase and suppressing homologous recombination; ortholog of human TopBP1; forms nuclear foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

TEL1

DNA-binding protein kinase TEL1, L000002281, YBL088C
Protein kinase primarily involved in telomere length regulation; contributes to cell cycle checkpoint control in response to DNA damage; acts with Red1p and Mec1p to promote interhomolog recombination by phosphorylation of Hop1; functionally redundant with Mec1p; regulates P-body formation induced by replication stress; homolog of human ataxia-telangiectasia mutated (ATM) gene, the gene responsible for ataxia telangiectasia (AT) (OMIM 607585)
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

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

Sensing of Replication Stress and Mec1 Activation Act through Two Independent Pathways Involving the 9-1-1 Complex and DNA Polymerase ε.

Puddu F, Piergiovanni G, Plevani P, Muzi-Falconi M

Following DNA damage or replication stress, budding yeast cells activate the Rad53 checkpoint kinase, promoting genome stability in these challenging conditions. The DNA damage and replication checkpoint pathways are partially overlapping, sharing several factors, but are also differentiated at various levels. The upstream kinase Mec1 is required to activate both signaling cascades together with the 9-1-1 PCNA-like complex and the ... [more]

PLoS Genet. Mar. 01, 2011; 7(3);e1002022 [Pubmed: 21436894]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: protein/peptide modification (APO:0000131)

Additional Notes

  • Deletion of tel1 prevents the residual p53 phosphorylation seen in ddc1 dpb11 double mutants.
  • The effect is also observable for each pair of mutants.

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
DPB11 TEL1
Synthetic Growth Defect
Synthetic Growth Defect

A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell.

Low-BioGRID
521224

Curated By

  • BioGRID