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Gene Review:

lin-3 - Protein LIN-3

Caenorhabditis elegans

Hwang, B.J. et al., Hwang, B.J. et al., Huang, L.S. et al., Ide, N. et al., Thompson, B.E. et al., et al.

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High impact information on lin-3

The lin-3 gene is necessary for induction of the Caenorhabditis elegans vulva by the anchor cell [1].
The LIN-3/EGF ligand may be the germ-line signal to the VPCs: the fog; fbf Muv phenotype depends on LIN-3 activity, and the lin-3 3' UTR possesses an FBF binding element [2].
We computationally identified egl-43 as a gene likely to be expressed in the pre-AC/pre-VU cells and the AC, based on the presence of an enhancer element similar to the one that transcribes lin-3 in the same cells [3].
A cell-specific enhancer that specifies lin-3 expression in the C. elegans anchor cell for vulval development [4].
Previous studies with lin-3 mutants and transgene expression have revealed that the level of LIN-3 in the AC must be precisely regulated for proper vulval development [4].

Biological context of lin-3

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 [5].
Mutagenesis studies show that both E-boxes and the NHR binding site are necessary to express lin-3 in the AC [4].

Anatomical context of lin-3

During C. elegans vulval development, the anchor cell (AC) in the somatic gonad expresses lin-3, activating the EGF receptor signaling pathway in vulval precursor cells (VPCs) and thereby inducing and patterning VPCs [4].
Here, we show that the SynMuv A and SynMuv B gene classes are functionally redundant for transcriptional repression of the key target gene, lin-3/EGF, in the hypodermis [6].

Associations of lin-3 with chemical compounds

Genes necessary for this induction include the lin-3 growth factor, the let-23 receptor tyrosine kinase, and let-60 ras. lin-15 is a negative regulator of this inductive pathway [7].

Other interactions of lin-3

A second extracellular cue, from Y.p, also acts antagonistically to the lin-3/let-23 pathway [8].
Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans [9].

References

The gene lin-3 encodes an inductive signal for vulval development in C. elegans. Hill, R.J., Sternberg, P.W. Nature (1992) [Pubmed]
Germ-line induction of the Caenorhabditis elegans vulva. Thompson, B.E., Lamont, L.B., Kimble, J. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
C. elegans EVI1 proto-oncogene, EGL-43, is necessary for Notch-mediated cell fate specification and regulates cell invasion. Hwang, B.J., Meruelo, A.D., Sternberg, P.W. Development (2007) [Pubmed]
A cell-specific enhancer that specifies lin-3 expression in the C. elegans anchor cell for vulval development. Hwang, B.J., Sternberg, P.W. Development (2004) [Pubmed]
Molecular cloning and characterization of rat lin-10. Ide, N., Hirao, K., Hata, Y., Takeuchi, M., Irie, M., Yao, I., Deguchi, M., Toyoda, A., Nishioka, H., Mizoguchi, A., Takai, Y. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
SynMuv Genes Redundantly Inhibit lin-3/EGF Expression to Prevent Inappropriate Vulval Induction in C. elegans. Cui, M., Chen, J., Myers, T.R., Hwang, B.J., Sternberg, P.W., Greenwald, I., Han, M. Dev. Cell (2006) [Pubmed]
The lin-15 locus encodes two negative regulators of Caenorhabditis elegans vulval development. Huang, L.S., Tzou, P., Sternberg, P.W. Mol. Biol. Cell (1994) [Pubmed]
The lin-3/let-23 pathway mediates inductive signalling during male spicule development in Caenorhabditis elegans. Chamberlin, H.M., Sternberg, P.W. Development (1994) [Pubmed]
Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans. Koga, M., Ohshima, Y. Mech. Dev. (1995) [Pubmed]

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