Format

Send to

Choose Destination
See comment in PubMed Commons below
Dev Biol. 2006 Jun 15;294(2):352-65. Epub 2006 May 3.

C. elegans Kallmann syndrome protein KAL-1 interacts with syndecan and glypican to regulate neuronal cell migrations.

Author information

  • 1Department of Molecular, Cell, and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, CA 95064, USA.

Abstract

The anosmin-1 protein family regulates cell migration, axon guidance, and branching, by mechanisms that are not well understood. We show that the C. elegans anosmin-1 ortholog KAL-1 promotes migrations of ventral neuroblasts prior to epidermal enclosure. KAL-1 does not modulate FGF signaling in neuroblast migration and acts in parallel to other neuroblast migration pathways. Defects in heparan sulfate (HS) synthesis or in specific HS modifications disrupt neuroblast migrations and affect the KAL-1 pathway. KAL-1 binds the cell surface HS proteoglycans syndecan/SDN-1 and glypican/GPN-1. This interaction is mediated via HS side chains and requires specific HS modifications. SDN-1 and GPN-1 are expressed in ventral neuroblasts and have redundant roles in KAL-1-dependent neuroblast migrations. Our findings suggest that KAL-1 interacts with multiple HSPGs to promote cell migration.

PMID:
16677626
DOI:
10.1016/j.ydbio.2006.02.036
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center