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A C. elegans Ror receptor tyrosine kinase regulates cell motility and asymmetric cell division

Author

Listed:
  • Wayne C. Forrester

    (Indiana University)

  • Megan Dell

    (University of California)

  • Elliot Perens

    (University of California)

  • Gian Garriga

    (University of California)

Abstract

Ror kinases are a family of orphan receptors with tyrosine kinase activity that are related to muscle specific kinase (MuSK), a receptor tyrosine kinase that assembles acetylcholine receptors at the neuromuscular junction1,2. Although the functions of Ror kinases are unknown, similarities between Ror and MuSK kinases have led to speculation that Ror kinases regulate synaptic development. Here we show that the Caenorhabditis elegans gene cam-1 encodes a member of the Ror kinase family that guides migrating cells and orients the polarity of asymmetric cell divisions and axon outgrowth. We find that tyrosine kinase activity is required for some of the functions of CAM-1, but not for its role in cell migration. CAM-1 is expressed in cells that require its function, and acts cell autonomously in migrating neurons. Overexpression and loss of cam-1 function result in reciprocal cell-migration phenotypes, indicating that levels of CAM-1 influence the final positions of migrating cells. Our results raise the possibility that Ror kinases regulate cell motility and asymmetric cell division in organisms as diverse as nematodes and mammals.

Suggested Citation

  • Wayne C. Forrester & Megan Dell & Elliot Perens & Gian Garriga, 1999. "A C. elegans Ror receptor tyrosine kinase regulates cell motility and asymmetric cell division," Nature, Nature, vol. 400(6747), pages 881-885, August.
  • Handle: RePEc:nat:nature:v:400:y:1999:i:6747:d:10.1038_23722
    DOI: 10.1038/23722
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    Cited by:

    1. Alon Kaufman & Gideon Dror & Isaac Meilijson & Eytan Ruppin, 2006. "Gene Expression of Caenorhabditis elegans Neurons Carries Information on Their Synaptic Connectivity," PLOS Computational Biology, Public Library of Science, vol. 2(12), pages 1-7, December.

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