BAIT

PFY1

CLS5, PRF1, profilin, L000001407, YOR122C
Profilin; binds actin, phosphatidylinositol 4,5-bisphosphate, and polyproline regions; involved in cytoskeleton organization; required for normal timing of actin polymerization in response to thermal stress; protein abundance increases in response to DNA replication stress; highly conserved protein; human PFN1 (profilin 1) complements temperature sensitive pfy1 mutants, PFN1 mutations are a rare cause of ALS
Saccharomyces cerevisiae (S288c)
PREY

RPN4

SON1, UFD5, stress-regulated transcription factor RPN4, L000001984, YDL020C
Transcription factor that stimulates expression of proteasome genes; Rpn4p levels are in turn regulated by the 26S proteasome in a negative feedback control mechanism; RPN4 is transcriptionally regulated by various stress responses; relative distribution to the nucleus increases upon DNA replication stress
Saccharomyces cerevisiae (S288c)

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.

Publication

Profilin 1 Associates with Stress Granules and ALS-Linked Mutations Alter Stress Granule Dynamics.

Figley MD, Bieri G, Kolaitis RM, Taylor JP, Gitler AD

Mutations in the PFN1 gene encoding profilin 1 are a rare cause of familial amyotrophic lateral sclerosis (ALS). Profilin 1 is a well studied actin-binding protein but how PFN1 mutations cause ALS is unknown. The budding yeast, Saccharomyces cerevisiae, has one PFN1 ortholog. We expressed the ALS-linked profilin 1 mutant proteins in yeast, demonstrating a loss of protein stability and ... [more]

J. Neurosci. Jun. 11, 2014; 34(24);8083-97 [Pubmed: 24920614]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: colony size (APO:0000063)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PFY1 RPN4
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.1659BioGRID
2016289

Curated By

  • BioGRID