Figure 3 | Signalling cascades.   a | The Ras signalling pathway is required for the formation of the vulva (the absence of the vulva is known as the vulvaless phenotype, Vul). The epidermal growth factor (EGF) ligand produced by the ANCHOR CELL binds the receptor tyrosine kinase on one or a few of the five vulval precursor cells, and initiates a signal-transduction cascade that culminates in the inactivation of the LIN-1 transcriptional inhibitor. Constitutive formation of the vulva by all of the vulval precursor cells can be caused by a gain-of-function (GOF) mutation in Ras or by loss-of-function (LOF) mutations in, for example, both lin-15a and lin-15b (the two lin-15 isoforms act redundantly). Constitutive activation of the Ras pathway causes the formation of pseudovulvae along the ventral surface (arrowheads; the arrow points to the true vulva). This multivulval (Muv) phenotype can be suppressed by lof mutations in downstream components of the pathway. b | The sex-determination pathway. The ratio of X chromosomes to autosomes (A) regulates the expression of the xol-1 gene. In hermaphrodites, which have two X chromosomes, a high X/A ratio inhibits xol-1 expression. In the absence of XOL-1 protein, the sdc genes are expressed. These genes inhibit the male-determining signal HER-1 and simultaneously activate the dosage-compensation genes. dpy, dumpy; ETS, E26 transformation defective; fem, feminization; GNRF, guanylyl-nucleotide-release factor; her, hermaphrodization; let, lethal; lin, abnormal cell lineage; map, mitogen-activated protein; mek, MAPK/ERK kinase; mpk, MAP kinase; raf, Ras-associated factor; sdc, sex determination and dosage compensation; sem, sex muscle abnormal; SOS, son of sevenless; tra, transformer; trx, transcription; xol, XO lethal.

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