BAIT

SGF73

SCA7, YGL066W
SAGA complex subunit; has a role in anchoring the deubiquitination module into SAGA and SLIK complexes; involved in preinitiation complex assembly at promoters; relocalizes to the cytosol in response to hypoxia; human ortholog ataxin-7 is associated with spinocerebellar ataxia diseases; mutant displays reduced transcription elongation in the G-less-based run-on (GLRO) assay
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 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

A novel role for Sem1 and TREX-2 in transcription involves their impact on recruitment and H2B deubiquitylation activity of SAGA.

Garcia-Oliver E, Pascual-Garcia P, Garcia-Molinero V, Lenstra TL, Holstege FC, Rodriguez-Navarro S

Transcription and mRNA export are linked processes. However, the molecular mechanisms of this coordination are not clear. Sus1 (hENY2) participates in this coordination as part of two protein complexes: SAGA, a transcriptional co-activator; TREX-2, which functions in mRNA biogenesis and export. Here, we investigate the coordinated action of SAGA and TREX-2 required for gene expression. We demonstrate that TREX-2 subunit ... [more]

Nucleic Acids Res. Jun. 01, 2013; 41(11);5655-68 [Pubmed: 23599000]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • SEM1 deletion were constructed in cells lacking GCN5, SGF73 and SUS1, absence of Sem1 leads to an enhancement of the poor growth exhibit by each single mutant, suggesting that these factors control the same biological function

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SGF73 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-5.4961BioGRID
217008
SGF73 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-5.378BioGRID
510605

Curated By

  • BioGRID