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

DUN1

serine/threonine protein kinase DUN1, L000000531, YDL101C
Cell-cycle checkpoint serine-threonine kinase; required for DNA damage-induced transcription of certain target genes, phosphorylation of Rad55p and Sml1p, and transient G2/M arrest after DNA damage; Mec1p and Dun1p function in same pathway to regulate both dNTP pools and telomere length; also regulates postreplicative DNA repair
Kinome Project (Sc)
GO Process (3)
GO Function (1)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

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

  • metabolism and growth (APO:0000094)
  • mutation frequency (APO:0000198)

Additional Notes

  • Dun1 inactivation partially suppresses the dNTP imbalance in ura7 and gln3 mutants
  • deletion of DUN1 almost completely suppressed the CAN1 mutator phenotype in pol1-L868M/gln3 double mutant
  • deletion of DUN1 almost completely suppressed the CAN1 mutator phenotype in pol3-L612M/ura7, pol2-04/gln3, and pol3-L612M/gln3 double mutants
  • genetic complex

Curated By

  • BioGRID