Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Axon guidance

The end of the branch

During neuronal development, axons form branches that allow a neuron to project to many targets. Colavita and Tessier-Lavigne have identified a signal in the worm Caenorhabditis elegans that acts as a branch-specific stop signal, giving new insight into how axonal branches are specified.

In C. elegans, a group of identified neurons — the VC neurons — form axonal branches at the vulva that travel a short way from the ventral nerve cord along the vulval epithelium before stopping. In the new study, Colavita and Tessier-Lavigne found that mutations in a particular gene, bam-2, cause the branches to overshoot so that they continue to extend across the vulval midline. bam-2 is expressed in a number of cells, including the vulval VulF cell, but not in the VC neurons.

The phenotype of bam-2 mutants could be rescued by expression of bam-2 in the VulF cell but not by expression in the VC neurons. The cytoplasmic domain of BAM-2 seems not to be needed for its branch-termination role, as a truncated bam-2 gene that lacked this domain could also rescue the phenotype. The sequence of the BAM-2 protein indicates that it is a cell-surface protein and is related to the neurexin family, members of which have been implicated in synaptogenesis.

Ectopic expression of bam-2 in the VC neurons of bam-2-null worms caused an interesting additional phenotype: in 43% of cases, one branch fascicle failed to form completely. Ectopic expression in a wild-type background did not have this effect. The authors propose that BAM-2 acts as a positive signal that attracts axon branches to the appropriate termination point: in the wild type, the normally expressed BAM-2 on the VulF cell overrides the effects of the transgene, but in the bam-2-null worms, ectopic expression in the neurons themselves interferes with branch extension.

The results of the study support the proposal that BAM-2 acts as a branch-termination signal for the VC axons. Surprisingly, it does not seem to influence termination of the primary axons; rather, it acts only on their branches. It seems likely that BAM-2 on the VulF cell acts as a ligand for a receptor that is localized to the VC axonal branches.

ORIGINAL RESEARCH PAPER

  1. Colavita, A. & Tessier-Lavigne, M. A neurexin-related protein, BAM-2, terminates axonal branches in C. elegans. Science 302, 293–296 (2003)

    CAS  Article  Google Scholar 

Download references

Authors

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Jones, R. The end of the branch. Nat Rev Neurosci 4, 935 (2003). https://doi.org/10.1038/nrn1291

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrn1291

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing