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Gene Review

lin-17  -  Protein LIN-17

Caenorhabditis elegans

 
 
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High impact information on lin-17

  • In Caenorhabditis elegans, mutations in lin-17, a Frizzled-class Wnt receptor, and in lin-18 affect cell fate patterning in the P7.p vulval lineage [1].
  • The son-1 mutation enhances the phenotypes of reduction-of-function lin-17 mutants in several developmental processes, including vulva development, somatic gonad development, and male tail patterning. son-1 encodes an HMG1/2-like DNA-binding protein and is localized in all cell nuclei through development as revealed by a GFP reporter construct [2].
  • The Caenorhabditis elegans gene lin-17, which is required for certain asymmetric cell divisions, encodes a putative seven-transmembrane protein similar to the Drosophila frizzled protein [3].
  • Studies using a lin-17-green fluorescent protein translational fusion indicate that lin-17 is expressed in mother cells before asymmetric cell divisions and in both daughter cells after the divisions [3].
  • In addition to ligand redundancy, we found that at least three Wnt receptors, lin-17, mom-5 and mig-1, function in the VPCs [4].
 

Biological context of lin-17

 

Anatomical context of lin-17

  • In lin-44/Wnt and lin-17/Frizzled mutants, the polarity of the PLM mechanosensory neuron is reversed along the body axis: the long PLM process, PLM growth cone, and synapses are posterior to its cell body instead of anterior [7].
 

Other interactions of lin-17

  • A mutation in lin-17 causes production of additional mec-3-expressing cells and can have its effect on the cell division that produces a mec-3-expressing cell [8].
  • We discuss the similarities and differences between the cellular defects seen in Rac mutants and let-60 Ras or lin-17 Frizzled mutants [9].
  • The POP-1 asymmetric distribution is controlled by lin-44 and lin-17 [10].
  • Analysis of lin-17;vab-3 double mutants suggests that vab-3 acts after lin-17 for B.a. fate specification [6].
  • Asymmetric distribution of nuclear GFP::POP-1 in Z1 and Z4 daughter cells is reversed in dsh-2 mutants, with higher levels in distal than proximal daughters. dsh-2 and the frizzled receptor homolog lin-17 have a strong genetic interaction, suggesting that they act in a common pathway [11].

References

  1. C. elegans LIN-18 is a Ryk ortholog and functions in parallel to LIN-17/Frizzled in Wnt signaling. Inoue, T., Oz, H.S., Wiland, D., Gharib, S., Deshpande, R., Hill, R.J., Katz, W.S., Sternberg, P.W. Cell (2004) [Pubmed]
  2. An HMG1-like protein facilitates Wnt signaling in Caenorhabditis elegans. Jiang, L.I., Sternberg, P.W. Genes Dev. (1999) [Pubmed]
  3. The Caenorhabditis elegans gene lin-17, which is required for certain asymmetric cell divisions, encodes a putative seven-transmembrane protein similar to the Drosophila frizzled protein. Sawa, H., Lobel, L., Horvitz, H.R. Genes Dev. (1996) [Pubmed]
  4. Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development. Gleason, J.E., Szyleyko, E.A., Eisenmann, D.M. Dev. Biol. (2006) [Pubmed]
  5. lin-17 mutations of Caenorhabditis elegans disrupt certain asymmetric cell divisions. Sternberg, P.W., Horvitz, H.R. Dev. Biol. (1988) [Pubmed]
  6. Mutations in the Caenorhabditis elegans gene vab-3 reveal distinct roles in fate specification and unequal cytokinesis in an asymmetric cell division. Chamberlin, H.M., Sternberg, P.W. Dev. Biol. (1995) [Pubmed]
  7. Wnt signals and frizzled activity orient anterior-posterior axon outgrowth in C. elegans. Hilliard, M.A., Bargmann, C.I. Dev. Cell (2006) [Pubmed]
  8. Regulation of anterior cell-specific mec-3 expression during asymmetric cell division in C. elegans. Way, J.C., Run, J.Q., Wang, A.Y. Dev. Dyn. (1992) [Pubmed]
  9. ced-10 Rac and mig-2 function redundantly and act with unc-73 trio to control the orientation of vulval cell divisions and migrations in Caenorhabditis elegans. Kishore, R.S., Sundaram, M.V. Dev. Biol. (2002) [Pubmed]
  10. tcl-2 encodes a novel protein that acts synergistically with Wnt signaling pathways in C. elegans. Zhao, X., Sawa, H., Herman, M.A. Dev. Biol. (2003) [Pubmed]
  11. DSH-2 regulates asymmetric cell division in the early C. elegans somatic gonad. Chang, W., Lloyd, C.E., Zarkower, D. Mech. Dev. (2005) [Pubmed]
 
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