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

DBP7

L000004205, YKR024C
Putative ATP-dependent RNA helicase of the DEAD-box family; involved in ribosomal biogenesis; required at post-transcriptional step for efficient retrotransposition; essential for growth under anaerobic conditions
GO Process (1)
GO Function (1)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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 DBP7
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-0.1742BioGRID
2016435

Curated By

  • BioGRID