BAIT

GLP-1

CELE_F02A9.6, emb-33, F02A9.6
glp-1 encodes an N-glycosylated transmembrane protein that, along with LIN-12, comprises one of two C. elegans members of the LIN-12/Notch family of receptors; from the N- to the C-terminus, GLP-1 is characterized by ten extracellular EGF-like repeats, three LIN-12/Notch repeats, a CC-linker, a transmembrane domain, a RAM domain, six intracellular ankyrin repeats, and a PEST sequence; in C. elegans, GLP-1 activity is required for cell fate specification in germline and somatic tissues; in the germline, GLP-1, acting as a receptor for the DSL family ligand LAG-2, is essential for mitotic proliferation of germ cells and maintenance of germline stem cells; in somatic tissues, maternally provided GLP-1, acting as a receptor for the DSL family ligand APX-1, is required for inductive interactions that specify the fates of certain embryonic blastomeres; GLP-1 is also required for some later embryonic cell fate decisions, and in these decisions its activity is functionally redundant with that of LIN-12; GLP-1 expression is regulated temporally and spatially via translational control, as GLP-1 mRNA, present ubiquitously in the germline and embryo, yields detectable protein solely in lateral, interior, and endomembranes of distal, mitotic germ cells, and then predominantly in the AB blastomere and its descendants in the early embryo; proper spatial translation of glp-1 mRNA in the embryo is dependent upon genes such as the par genes, that are required for normal anterior-posterior asymmetry in the early embryo; signaling through GLP-1 controls the activity of the downstream Notch pathway components LAG-3 and LAG-1, the latter being predicted to function as part of a transcriptional feedback mechanism that positively regulates GLP-1 expression; signaling through the DNA-binding protein LAG-1 is believed to involve a direct interaction between LAG-1 and the GLP-1 RAM and ankyrin domains
Caenorhabditis elegans
PREY

LAG-2

CELE_Y73C8B.4, let-461, sel-3, Y73C8B.4
lag-2 encodes a transmembrane protein of the Delta/Serrate/Lag-2 (DSL) family that functions as a signaling ligand for the GLP-1 and LIN-12 Notch-like receptors; LAG-2 is required for larval viability and for cell fate decisions involving the germline (meiosis vs mitosis), the somatic gonad, and the early embryo; in addition, LAG-2 functions redundantly with the transmembrane APX-1 and secreted DSL-1 ligands to regulate lateral signaling during vulval development; LAG-2 is expressed in the distal tip cell of the somatic gonad, the ventral nerve cord, the descendants of ABalap and MSap in the developing embryo, and in all six vulval precursor cells (VPCs) during the early L3 stage, with later expression in the VPCs generally restricted to P6.p; lag-2 expression in the vulval cells is regulated by the LET-23/EGF receptor signaling pathway and the SUR-2 component of the Mediator transcription complex.
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

  • 4.375 [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