BAIT

PRP8

DBF3, DNA39, RNA8, SLT21, USA2, U4/U6-U5 snRNP complex component PRP8, L000001500, L000003226, YHR165C
Component of U4/U6-U5 snRNP complex; involved in second catalytic step of splicing; participates in spliceosomal assembly through its interaction with U1 snRNA; largest and most evolutionarily conserved protein of the spliceosome; mutations in its human ortholog, PRPF8, cause Retinitis pigmentosa and missplicing in Myelodysplastic syndrome.
Saccharomyces cerevisiae (S288c)
PREY

YHC1

U1C, U1-C, L000004161, YLR298C
Component of the U1 snRNP complex required for pre-mRNA splicing; putative ortholog of human U1C protein, which is involved in formation of a complex between U1 snRNP and the pre-mRNA 5' splice site
GO Process (2)
GO Function (2)
GO Component (3)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

An unanticipated early function of DEAD-box ATPase Prp28 during commitment to splicing is modulated by U5 snRNP protein Prp8.

Price AM, Goernemann J, Guthrie C, Brow DA

The stepwise assembly of the highly dynamic spliceosome is guided by RNA-dependent ATPases of the DEAD-box family, whose regulation is poorly understood. In the canonical assembly model, the U4/U6.U5 triple snRNP binds only after joining of the U1 and, subsequently, U2 snRNPs to the intron-containing pre-mRNA. Catalytic activation requires the exchange of U6 for U1 snRNA at the 5' splice ... [more]

RNA Jan. 01, 2014; 20(1);46-60 [Pubmed: 24231520]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • Figure 2
  • genetic complex
  • yhc1-1 expression bypasses prp28 prp8 double mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PRP8 YHC1
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-0.1865BioGRID
2048197

Curated By

  • BioGRID