BAIT

GLN3

nitrogen-responsive transcriptional regulator GLN3, L000000710, YER040W
Transcriptional activator of genes regulated by nitrogen catabolite repression; localization and activity regulated by quality of nitrogen source and Ure2p
Saccharomyces cerevisiae (S288c)
PREY

MSH2

PMS5, mismatch repair ATPase MSH2, L000001190, YOL090W
Protein that binds to DNA mismatches; forms heterodimers with Msh3p and Msh6p that bind to DNA mismatches to initiate the mismatch repair process; contains a Walker ATP-binding motif required for repair activity and involved in interstrand cross-link repair; Msh2p-Msh6p binds to and hydrolyzes ATP
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

Alterations in cellular metabolism triggered by URA7 or GLN3 inactivation cause imbalanced dNTP pools and increased mutagenesis.

Schmidt TT, Reyes G, Gries K, Ceylan C Ue, Sharma S, Meurer M, Knop M, Chabes A, Hombauer H

Eukaryotic DNA replication fidelity relies on the concerted action of DNA polymerase nucleotide selectivity, proofreading activity, and DNA mismatch repair (MMR). Nucleotide selectivity and proofreading are affected by the balance and concentration of deoxyribonucleotide (dNTP) pools, which are strictly regulated by ribonucleotide reductase (RNR). Mutations preventing DNA polymerase proofreading activity or MMR function cause mutator phenotypes and consequently increased cancer ... [more]

Proc. Natl. Acad. Sci. U.S.A. May. 30, 2017; 114(22);E4442-E4451 [Pubmed: 28416670]

Throughput

  • Low Throughput

Ontology Terms

  • mutation frequency (APO:0000198)

Additional Notes

  • double mutants show increased mutator phenotypes

Curated By

  • BioGRID