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

MSH6

PMS3, PMS6, mismatch repair ATPase MSH6, L000003135, L000004503, S000029377, YDR097C
Protein required for mismatch repair in mitosis and meiosis; forms a complex with Msh2p to repair both single-base & insertion-deletion mispairs; also involved in interstrand cross-link repair; potentially phosphorylated by Cdc28p
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