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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

slt-1  -  Protein SLT-1

Caenorhabditis elegans

 
 
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High impact information on slt-1

  • Surprisingly, slt-1 mutants do not exhibit the nerve ring and epithelial defects of sax-3 mutants, suggesting that SAX-3 has both Slit-dependent and Slit-independent functions in development [1].
  • A double-mutant combination between vab-1 and slt-1 unmasks a role for the SLT-1 ligand in embryogenesis [2].
  • We show here that loss-of-function mutations in clr-1 enhance netrin-dependent attraction, suppressing ventral guidance defects in slt-1 mutants. clr-1 encodes a transmembrane receptor protein tyrosine phosphatase (RPTP) that functions in AVM to inhibit signaling through the DCC family receptor UNC-40 and its effector, UNC-34/enabled [3].

References

  1. C. elegans slit acts in midline, dorsal-ventral, and anterior-posterior guidance via the SAX-3/Robo receptor. Hao, J.C., Yu, T.W., Fujisawa, K., Culotti, J.G., Gengyo-Ando, K., Mitani, S., Moulder, G., Barstead, R., Tessier-Lavigne, M., Bargmann, C.I. Neuron (2001) [Pubmed]
  2. The VAB-1 Eph receptor tyrosine kinase and SAX-3/Robo neuronal receptors function together during C. elegans embryonic morphogenesis. Ghenea, S., Boudreau, J.R., Lague, N.P., Chin-Sang, I.D. Development (2005) [Pubmed]
  3. Inhibition of netrin-mediated axon attraction by a receptor protein tyrosine phosphatase. Chang, C., Yu, T.W., Bargmann, C.I., Tessier-Lavigne, M. Science (2004) [Pubmed]
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