BAIT

LET-60

CELE_ZK792.6, lin-34, ZK792.6
let-60 encodes a member of the GTP-binding RAS protooncogene family; let-60 activity is required for viability, vulval development, spicule development, germ line meiotic progression, posterior development of the hypodermis, chemotaxis, sex myoblast migration, and muscle membrane extension; let-60 acts genetically downstream of let-23 with respect to vulval development and upstream of the MAPK pathway with respect to chemotaxis; let-60 is expressed in neural, muscle, and hypodermal lineages.
Caenorhabditis elegans
PREY

KSR-1

CELE_F13B9.5, sur-3, sar-2, F13B9.5
ksr-1 encodes one of two C. elegans Kinase Suppressor of Ras paralogs; during development, ksr-1 functions singly to control sex myoblast migration and redundantly with ksr-2 to control development of the vulva, excretory system, and male spicules; as ksr-2; ksr-1 doubly mutant animals have severely reduced or absent MPK-1/ERK diphosphorylation levels in somatic tissue, KSR-2 and KSR-1 likely function to positively regulate signaling through the LET-60/Ras pathway; genetic analyses have identified a number of ekl (enhancer of ksr-1 lethality ) mutations that, in combination with a ksr-1 null mutation, result in defects in excretory duct cell fate specification accompanied by larval lethality; the ekl mutations identified gene products that are maternally required for duct cell fate specification and encode proteins likely to be involved in transcriptional and post-transcriptional gene regulation.
Caenorhabditis elegans

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.

Publication

A global analysis of genetic interactions in Caenorhabditis elegans.

Byrne AB, Weirauch MT, Wong V, Koeva M, Dixon SJ, Stuart JM, Roy PJ

BACKGROUND: Understanding gene function and genetic relationships is fundamental to our efforts to better understand biological systems. Previous studies systematically describing genetic interactions on a global scale have either focused on core biological processes in protozoans or surveyed catastrophic interactions in metazoans. Here, we describe a reliable high-throughput approach capable of revealing both weak and strong genetic interactions in the ... [more]

J. Biol. Sep. 28, 2007; 6(3);8 [Pubmed: 17897480]

Quantitative Score

  • 1.75 [SGA Score]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: organism development variant (WBPHENOTYPE:0000531)

Additional Notes

  • A systematic genetic interaction analysis (SGI) was carried out to detect interactions between 11 query mutants and 858 target genes compromised by RNA interference (RNAi). Interactions were determined using growth scores that indicated whether the resulting number of progeny from the double mutant was significantly different than that of single mutant controls.
  • Negative Genetic

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
KSR-1 LET-60
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.

High-BioGRID
467247
LET-60 KSR-1
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.

High-BioGRID
467295

Curated By

  • BioGRID