lgd, l(2)gd, lethal (2) giant discs, lethal giant discs, gd
Gene model reviewed during 5.52
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\l(2)gd1 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\l(2)gd1 in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
dsRNA has been made from templates generated with primers directed against this gene.
The l(2)gd1 product regulates N signaling in a manner that is independent of the N ligands, Dl and Ser. The genetic interaction between l(2)gd1 and Hrs, and the accumulation of N protein in subcellular puncta suggests that l(2)gd1 has a role in N protein trafficking.
Tumor suppressor genes act in combination to control cell proliferation. Tissue hyperplasia can be associated with ectopic expression of genes involved in pattern formation. The enhancement of leg disc duplication in l(2)gd1 mutants by ft is mediated by dpp.
Mutants display hyperplastic phenotype, with imaginal disc overgrowth.
Endocrine mechanisms responsible for the prolongation of larval life in l(2)gd1 mutants were investigated: results suggest that delayed pupariation is caused by the overgrown imaginal discs inhibiting the production or release of ecdysteroids from the endocrine system.
Mutants at l(2)gd1 exhibit hyperplastic overgrowth.