BAIT

RTC1

SEA2, YOL138C
Subunit of the SEA (Seh1-associated) complex; SEA is a coatomer-related complex that associates dynamically with the vacuole; null mutation suppresses cdc13-1 temperature sensitivity; has N-terminal WD-40 repeats and a C-terminal RING motif
GO Process (0)
GO Function (0)
GO Component (4)
Saccharomyces cerevisiae (S288c)
PREY

FPR4

peptidylprolyl isomerase FPR4, L000004352, YLR449W
Peptidyl-prolyl cis-trans isomerase (PPIase); nuclear proline isomerase; affects expression of multiple genes via its role in nucleosome assembly; catalyzes isomerization of proline residues in histones H3 and H4, which affects lysine methylation of those histones; PPIase domain acts as a transcriptional repressor when tethered to DNA by lexA, and repressor activity is dependent on PPIase activity; FPR4 has a paralog, FPR3, that arose from the whole genome duplication
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

Molecular architecture and function of the SEA complex, a modulator of the TORC1 pathway.

Algret R, Fernandez-Martinez J, Shi Y, Kim SJ, Pellarin R, Cimermancic P, Cochet E, Sali A, Chait BT, Rout MP, Dokudovskaya S

The TORC1 signaling pathway plays a major role in the control of cell growth and response to stress. Here we demonstrate that the SEA complex physically interacts with TORC1 and is an important regulator of its activity. During nitrogen starvation, deletions of SEA complex components lead to Tor1 kinase delocalization, defects in autophagy, and vacuolar fragmentation. TORC1 inactivation, via nitrogen ... [more]

Mol. Cell Proteomics Nov. 01, 2014; 13(11);2855-70 [Pubmed: 25073740]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RTC1 FPR4
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-0.1365BioGRID
2180865

Curated By

  • BioGRID