BAIT

DRN1

YGR093W
Splicing factor that modulates turnover of branched RNAs by Dbr1p; interacts with spliceosomal components and branched RNA splicing products; enhances Dbr1p debranching in vitro; conserved protein with domain organization identical from yeast to human; N-terminal homology to Dbr1p N-terminus, but Dbr1p catalytic residues not conserved; relocalizes to the cytosol in response to hypoxia
GO Process (1)
GO Function (2)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

SYF1

NTC90, L000004195, YDR416W
Member of the NineTeen Complex (NTC); that contains Prp19p and stabilizes U6 snRNA in catalytic forms of the spliceosome containing U2, U5, and U6 snRNAs; null mutant has splicing defect and arrests in G2/M; relocalizes to the cytosol in response to hypoxia; homologs in human and C. elegans
Saccharomyces cerevisiae (S288c)

Two-hybrid

Bait protein expressed as a DNA binding domain (DBD) fusion and prey expressed as a transcriptional activation domain (TAD) fusion and interaction measured by reporter gene activation.

Publication

A homolog of lariat-debranching enzyme modulates turnover of branched RNA.

Garrey SM, Katolik A, Prekeris M, Li X, York K, Bernards S, Fields S, Zhao R, Damha MJ, Hesselberth JR

Turnover of the branched RNA intermediates and products of pre-mRNA splicing is mediated by the lariat-debranching enzyme Dbr1. We characterized a homolog of Dbr1 from Saccharomyces cerevisiae, Drn1/Ygr093w, that has a pseudo-metallophosphodiesterase domain with primary sequence homology to Dbr1 but lacks essential active site residues found in Dbr1. Whereas loss of Dbr1 results in lariat-introns failing broadly to turnover, loss ... [more]

RNA Jun. 11, 2014; 0(0); [Pubmed: 24919400]

Throughput

  • Low Throughput

Additional Notes

  • Figure 2

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
DRN1 SYF1
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-0.1532BioGRID
2045006

Curated By

  • BioGRID