BAIT

BAR-1

CELE_C54D1.6, pvl-1, spy-1, C54D1.6
bar-1 encodes a beta-catenin; during C. elegans development, BAR-1 likely functions as a transcriptional coactivator whose activity is required for Q neuroblast migration, P12 cell fate specification, and P3.p through P8.p vulval cell fate specification at two different stages of development; in specifying vulval cell fates, bar-1 interacts with Wnt and MAPK signaling pathways to regulate proper expression of the LIN-39 homeodomain transcription factor, overexpresion of which can partially rescue the bar-1 mutant phenotype; in yeast two-hybrid assays, BAR-1 interacts strongly with the POP-1/TCF transcription factor, and when fused to the Gal4 DNA binding domain, BAR-1 can function in yeast as a transcriptional coactivator; during larval development, BAR-1 expression begins in P3.p through P8.p at the late L1 stage and then disappears from these cells by the mid-L3 stage; BAR-1 is also expressed in P12, in the seam cells, and in cells of the somatic gonad; BAR-1 subcellular localization, assessed using an integrated transgene, reveals localization to the cytoplasm, nucleus, and cell junctions; genetic mosaic analyses indicate that, in P4.p and in P12, bar-1 acts cell autonomously to specify cell fates.
Caenorhabditis elegans
PREY

LET-502

CELE_C10H11.9, C10H11.9
let-502 encodes a Rho-binding Ser/Thr kinase orthologous to human myotonic dystrophy kinase (DM-kinase); let-502 is required for early embryonic cleavages, embryonic elongation, migration of hypodermal P cells to a ventral position, normal spermathecal contraction, and fertility; LET-502 is required for hypodermal cells to properly change their shape, and is expressed in those cells, during embryonic elongation; let-502 mutations are suppressed by mel-11 mutations, and the pattern of LET-502 expression in the embryonic epidermis and the spermatheca is opposite to that of MEL-11, indicating that LET-502 and MEL-11 have opposing functions (presumably tissue contraction and relaxation); MEL-11 requires LET-502 (along with the nonmuscle myosin NMY-1) for proper localization.
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

  • 3.2857 [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

Curated By

  • BioGRID