A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

Transmembrane insertases and N-glycosylation critically determine synthesis, trafficking, and activity of the nonselective cation channel TRPC6.

Talbot BE, Vandorpe DH, Stotter BR, Alper SL, Schlondorff JS

Transient receptor potential cation channel subfamily C member 6 (TRPC6) is a widely expressed ion channel. Gain-of-function mutations in the human TRPC6 channel cause autosomal-dominant focal segmental glomerulosclerosis, but the molecular components involved in disease development remain unclear. Here, we found that overexpression of gain-of-function TRPC6 channel variants is cytotoxic in cultured cells. Exploiting this phenotype in a genome-wide CRISPR/Cas ... [more]

J. Biol. Chem. Aug. 23, 2019; 294(34);12655-12669 [Pubmed: 31266804]

Throughput

Low Throughput

Ontology Terms

phenotype: growth abnormality (HP:0001507)
phenotype: viability (PATO:0000169)

Additional Notes

CRISPR GI
Cell Line: HEK 293
TRPC6 GOF mutants are cytotoxic in a variety of cells and MGAT1 knockout can rescue this cytotoxicity in a cell line specific manner

Related interactions

Interaction	Experimental Evidence Code	Dataset	Throughput	Score	Curated By	Notes
TRPC6 MGAT1	Positive Genetic Positive Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.	Talbot BE (2019)	High	-	BioGRID	2606590

Curated By

BioGRID

Interaction Summary

TRPC6

Gene Ontology Biological Process

Gene Ontology Molecular Function

inositol 1,4,5 trisphosphate binding [IDA]protein binding [IPI]

Gene Ontology Cellular Component

MGAT1