A role for septins in cellular and axonal migration in C. elegans.

Dev Biol

Laboratory of Molecular Biology, University of Wisconsin, 1525 Linden Drive, Madison, WI 53706, USA.

Published: September 2003

AI Article Synopsis

  • Caenorhabditis elegans has genes unc-59 and unc-61 that are part of the septin family and mutations in these genes lead to locomotion issues, previously linked to problems during cell division in nerve cells.
  • New findings show that these mutations also cause uncoordination in newly hatched larvae without affecting cytokinesis.
  • The study highlights that septins are crucial for neuronal development and migratory processes, impacting axonal guidance and the morphology of cells involved in gonad development.

Article Abstract

Caenorhabditis elegans has two genes, unc-59 and unc-61, encoding septin-family GTPases. Mutations in the septin genes cause defects in locomotory behavior that have been previously attributed to cytokinesis failures in postembryonic neuroblasts. We find that mutations in either septin gene frequently cause uncoordination in newly hatched larvae in the absence of cytokinesis failures. The septins exhibit developmentally regulated expression, including expression in various neurons at times when processes are extending and synapses are forming. Motor neurons in the mutant larvae display defects in multiple aspects of axonal migration and guidance that are likely to be responsible for the locomotory behavior defects. The septins are also expressed in migrating distal tip cells, which are leaders for gonad arm extension. Septin mutants affect morphology of the distal tip cells, as well as their migration and guidance during gonadogenesis. These results suggest that septins may be generally required for developmental migrations and pathfinding.

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http://dx.doi.org/10.1016/s0012-1606(03)00296-3DOI Listing

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