BAIT

BMH1

APR6, 14-3-3 family protein BMH1, L000000185, YER177W
14-3-3 protein, major isoform; controls proteome at post-transcriptional level, binds proteins and DNA, involved in regulation of exocytosis, vesicle transport, Ras/MAPK and rapamycin-sensitive signaling, aggresome formation, spindle position checkpoint; protein increases in abundance and relative distribution to the nucleus increases upon DNA replication stress; antiapoptotic gene similar to human 14-3-3; BMH1 has a paralog, BMH2, that arose from whole genome duplication
Saccharomyces cerevisiae (S288c)
PREY

GCN4

AAS101, AAS3, ARG9, amino acid starvation-responsive transcription factor GCN4, L000000683, YEL009C
bZIP transcriptional activator of amino acid biosynthetic genes; activator responds to amino acid starvation; expression is tightly regulated at both the transcriptional and translational levels
Saccharomyces cerevisiae (S288c)

Synthetic Lethality

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

Publication

Deleting the 14-3-3 protein Bmh1 extends life span in Saccharomyces cerevisiae by increasing stress response.

Wang C, Skinner C, Easlon E, Lin SJ

Enhanced stress response has been suggested to promote longevity in many species. Calorie restriction (CR) and conserved nutrient-sensing target of rapamycin (TOR) and protein kinase A (PKA) pathways have also been suggested to extend life span by increasing stress response, which protects cells from age-dependent accumulation of oxidative damages. Here we show that deleting the yeast 14-3-3 protein, Bmh1, extends ... [more]

Genetics Dec. 01, 2009; 183(4);1373-84 [Pubmed: 19805817]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Curated By

  • BioGRID