You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Abstract
The nematode Caenorhabditis elegans is emerging as a promising model for studying the molecular control of axon regeneration. A forward genetic screen identified the DLK-1 (dual leucine zipper-bearing kinase 1) MAP (mitogen-activated protein) kinase pathway as a positive regulator of growth cone formation during axon regeneration. Although DLK-1 pathway mutant animals display a dramatic defect in regeneration, their axons have no apparent defects in initial outgrowth. The DLK-1 pathway also plays a role in synaptogenesis, but this role appears to be separate from its function in regeneration. Understanding how the DLK-1 pathway acts in development, plasticity, and regeneration may shed light on the evolution of mechanisms regulating axon regeneration.
