BAIT

SCC2

L000004262, YDR180W
Subunit of cohesin loading factor (Scc2p-Scc4p); a complex required for loading of cohesin complexes onto chromosomes; involved in establishing sister chromatid cohesion during DSB repair via histone H2AX; evolutionarily-conserved adherin; relocalizes to the cytosol in response to hypoxia
Saccharomyces cerevisiae (S288c)
PREY

SEN1

CIK3, NRD2, putative DNA/RNA helicase SEN1, L000001862, YLR430W
Presumed helicase and subunit of the Nrd1 complex (Nrd1p-Nab3p-Sen1p); complex interacts with the exosome to mediate 3' end formation of some mRNAs, snRNAs, snoRNAs, and CUTs; has a separate role in coordinating DNA replication with transcription, by associating with moving replication forks and preventing errors that occur when forks encounter transcribed regions; homolog of Senataxin, which is implicated in Ataxia-Oculomotor Apraxia 2 and a dominant form of ALS
Saccharomyces cerevisiae (S288c)

Affinity Capture-MS

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.

Publication

Mediator recruits the cohesin loader Scc2 to RNA Pol II-transcribed genes and promotes sister chromatid cohesion.

Mattingly M, Seidel C, Munoz S, Hao Y, Zhang Y, Wen Z, Florens L, Uhlmann F, Gerton JL

The ring-like cohesin complex plays an essential role in chromosome segregation, organization, and double-strand break repair through its ability to bring two DNA double helices together. Scc2 (NIPBL in humans) together with Scc4 functions as the loader of cohesin onto chromosomes. Chromatin adapters such as the RSC complex facilitate the localization of the Scc2-Scc4 cohesin loader. Here, we identify a ... [more]

Curr Biol Dec. 11, 2021; 32(13);2884-2896.e6 [Pubmed: 35654035]

Throughput

  • High Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SCC2 SEN1
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-0.1396BioGRID
1926154

Curated By

  • BioGRID