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.

Publication

Systematic screen for mutants resistant to TORC1 inhibition in fission yeast reveals genes involved in cellular ageing and growth.

Rallis C, Lopez-Maury L, Georgescu T, Pancaldi V, Baehler J

Target of rapamycin complex 1 (TORC1), which controls growth in response to nutrients, promotes ageing in multiple organisms. The fission yeast Schizosaccharomyces pombe emerges as a valuable genetic model system to study TORC1 function and cellular ageing. Here we exploited the combinatorial action of rapamycin and caffeine, which inhibit fission yeast growth in a TORC1-dependent manner. We screened a deletion ... [more]

Biol Open Jan. 24, 2014; 0(0); [Pubmed: 24463365]

Throughput

High Throughput

Related interactions

Interaction	Experimental Evidence Code	Dataset	Throughput	Score	Curated By	Notes
SCK2 SCK1	Phenotypic Enhancement Phenotypic Enhancement A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.	Chen BR (2009)	Low	-	PomBase	-
SCK1 SCK2	Phenotypic Enhancement Phenotypic Enhancement A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.	Fujita M (1998)	Low	-	BioGRID	798191

Curated By

BioGRID

Interaction Summary

SCK2

Gene Ontology Biological Process

Gene Ontology Cellular Component

SCK1