BAIT

ERD1

LDB2, L000000566, L000004741, YDR414C
Predicted membrane protein required for lumenal ER protein retention; mutants secrete the endogenous ER protein, BiP (Kar2p)
GO Process (2)
GO Function (0)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

ELO3

SUR4, APA1, SRE1, VBM1, fatty acid elongase ELO3, L000002245, YLR372W
Elongase; involved in fatty acid and sphingolipid biosynthesis; synthesizes very long chain 20-26-carbon fatty acids from C18-CoA primers; involved in regulation of sphingolipid biosynthesis
GO Process (0)
GO Function (0)
GO Component (0)
Saccharomyces cerevisiae (S288c)

Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Publication

Comprehensive characterization of genes required for protein folding in the endoplasmic reticulum.

Jonikas MC, Collins SR, Denic V, Oh E, Quan EM, Schmid V, Weibezahn J, Schwappach B, Walter P, Weissman JS, Schuldiner M

Protein folding in the endoplasmic reticulum is a complex process whose malfunction is implicated in disease and aging. By using the cell's endogenous sensor (the unfolded protein response), we identified several hundred yeast genes with roles in endoplasmic reticulum folding and systematically characterized their functional interdependencies by measuring unfolded protein response levels in double mutants. This strategy revealed multiple conserved ... [more]

Science Mar. 27, 2009; 323(5922);1693-7 [Pubmed: 19325107]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: protein/peptide accumulation (APO:0000149)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
ERD1 ELO3
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-0.189BioGRID
370543
ERD1 ELO3
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-0.2044BioGRID
2101638
ELO3 ERD1
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-5.4387BioGRID
580580
ERD1 ELO3
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-8.6717BioGRID
897722
ERD1 ELO3
PCA
PCA

A Protein-Fragment Complementation Assay (PCA) is a protein-protein interaction assay in which a bait protein is expressed as fusion to one of the either N- or C- terminal peptide fragments of a reporter protein and prey protein is expressed as fusion to the complementary N- or C- terminal fragment of the same reporter protein. Interaction of bait and prey proteins bring together complementary fragments, which can then fold into an active reporter, e.g. the split-ubiquitin assay.

High-BioGRID
433623
ELO3 ERD1
Phenotypic Suppression
Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

High-BioGRID
459478

Curated By

  • BioGRID