BAIT

SPT8

SAGA complex subunit SPT8, L000002034, YLR055C
Subunit of the SAGA transcriptional regulatory complex; not present in SAGA-like complex SLIK/SALSA; required for SAGA-mediated inhibition at some promoters
Saccharomyces cerevisiae (S288c)
PREY

SEM1

DSS1, HOD1, proteasome regulatory particle lid subunit SEM1, L000003539, L000004647, YDR363W-A
Component of lid subcomplex of 26S proteasome regulatory subunit; involved in mRNA export mediated by TREX-2 complex (Sac3p-Thp1p); assumes different conformations in different contexts, functions as molecular glue stabilizing the Rpn3p/Rpn7p regulatory heterodimer, and tethers it to lid helical bundle; ortholog of human DSS1; protein abundance increases in response to DNA replication stress
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

H2B ubiquitin protease Ubp8 and Sgf11 constitute a discrete functional module within the Saccharomyces cerevisiae SAGA complex.

Ingvarsdottir K, Krogan NJ, Emre NC, Wyce A, Thompson NJ, Emili A, Hughes TR, Greenblatt JF, Berger SL

The SAGA complex is a multisubunit protein complex involved in transcriptional regulation in Saccharomyces cerevisiae. SAGA combines proteins involved in interactions with DNA-bound activators and TATA-binding protein (TBP), as well as enzymes for histone acetylation (Gcn5) and histone deubiquitylation (Ubp8). We recently showed that H2B ubiquitylation and Ubp8-mediated deubiquitylation are both required for transcriptional activation. For this study, we investigated ... [more]

Mol. Cell. Biol. Feb. 01, 2005; 25(3);1162-72 [Pubmed: 15657441]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SPT8 SEM1
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-8.7318BioGRID
510549

Curated By

  • BioGRID