High impact information on let-23

• Furthermore, compensatory mutations in lin-7 and let-23 exhibit allele-specific suppression of apical mislocalization and signaling-defective phenotypes [1].
• The let-23 receptor/mpk-1 MAP kinase signaling pathway induces the vulva in C. elegans [2].
• Many genes required for vulval induction have been identified, including the let-23 receptor tyrosine kinase gene and the let-60 ras gene [3].
• It is shown that let-23 encodes a putative tyrosine kinase of the epidermal growth factor receptor subfamily [4].
• The let-23 gene is required for induction of the Caenorhabditis elegans vulva [4].

Biological context of let-23

• The sli-1 locus displays dosage sensitivity: severe reduction of function alleles of sli-1 are semidominant suppressors; a duplication of the sli-1(+) region enhances the vulvaless phenotype of hypomorphic mutations of let-23 [5].
• Our genetic epistasis experiments suggest that sli-3 functions either downstream or in parallel to nuclear factors lin-1 and sur-2. sli-3 synergistically interacts with the previously identified negative regulators of the let-23 signaling pathway and causes excessive cell proliferation [6].
• In Caenorhabditis elegans, the vulval induction is mediated by tyrosine kinase receptor/Ras signal transduction pathway composed of the lin-3, let-23, and let-60 products [7].
• We find that sem-5 also has a negative function in let-23-mediated ovulation and suggest that this negative function is mediated by the recruitment of inhibitors such as ARK-1 [8].
• The penetrance of the multivulva phenotype caused by loss-of-function mutations in lin-15, and gain-of-function mutations in let-23 or let-60 ras, was reduced by ptp-2(op194) [9].

Anatomical context of let-23

• The let-60 gene of Caenorhabditis elegans controls the choice between vulval and hypodermal differentiation in response to an inductive signal from the gonad. let-60 encodes a ras protein that acts downstream of the let-23 receptor tyrosine kinase in a signal transduction pathway [10].

Physical interactions of let-23

• The product of C. elegans lin-7 directly interacts with let-23 RTK and localize it at epithelial junctions [11].

Other interactions of let-23

• A second extracellular cue, from Y.p, also acts antagonistically to the lin-3/let-23 pathway [12].
• Inhibition of Caenorhabditis elegans vulval induction by gap-1 and by let-23 receptor tyrosine kinase [13].
• Reduction-of-function mutations in two Caenorhabditis elegans genes, the receptor tyrosine kinase gene let-23 and the collagen gene dpy-10, both alter the AG at the end of a short (ca. 50-nucleotide) intron to AA [14].
• The temporal and spatial expression of IPP-5 is consistent with its proposed inhibition of IP(3) signaling in the adult spermatheca. ipp-5 acts downstream of let-23, and interacts with let-23-mediated IP(3) signaling pathway genes [15].
• The precise localization of the let-23 RTK at the epithelial junctions is essential for the vulval induction, and requires three genes including lin-2, -7, and -10 [11].

Analytical, diagnostic and therapeutic context of let-23

• The 5' end of the let-23 mRNA was mapped by sequencing polymerase chain reaction products, and two mRNAs were found which had alternative exons and were probably initiated at different sites [16].

References