Different levels of the C. elegans growth factor LIN-3 promote distinct vulval precursor fates

Article Abstract:

The epidermal growth factor-like domain of the LIN-3 protein can stimulate a 1 degree fate and a lower dose of LIN-3 stimulates a 2 degree fate. A big amount of LIN-3 can also stimulate neighbouring vulval precursor cells to attain 1 degree fates. Thus, a high degree of LIN-3 can overrule the lateral signaling that usually precludes creation of adjacent 1 degree fates. It is proposed that the unchangeable pattern of vulval cell fates is produced by a graded distribution of LIN-3 that advances various vulval fates according to local concentration and by a lateral signal strengthening the primary bias.

Vulva

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Inositol triphosphate mediates a RAS-independent response to LET-23 receptor tyrosine kinase activation in C. elegans

Article Abstract:

Research was conducted to examine whether an inositol trisphosphate receptor can function as a RAS-independent, tissue-specific positive effector of LET-23, the Caenorhabditis elegans homology of the epidermal growth factor receptor. Transgenic strains were produced by standard methods while tissue-specific suppressors were isolated by screening F2 progeny of mutagenized hermaphrodites. Results identified mutations in two loci as tissue-specific suppressors of reduced LIN-3/LET-23-mediated signaling.

Analysis, Physiological aspects, Epidermal growth factor, Epidermal growth factors, Inositol phosphates

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sli-1, a negative regulator of let-23-mediated signaling in C. elegans

Article Abstract:

The 12 mutations which define the suppressor of lineage defect-1 (sli-1) locus is recovered by screening for the suppressors of hypomorphic mutations of let-23. The let -23 is a receptor kinase essential for vulval induction in Caenorhabditis elegans. Five phenotypes related to the hypomorphic alleles of let-23 by sli-1.

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