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First published online February 22, 2008
doi: 10.1242/10.1242/dev.013995

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Distinct cellular and molecular mechanisms mediate initial axon development and adult-stage axon regeneration in C. elegans

¹ Department of Physics and Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
² Department of Biology and Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 1B1, Canada.
³ Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

^* Authors for correspondence (e-mails: chieh.chang{at}mcgill.ca; samuel{at}physics.harvard.edu)

Accepted 2 January 2008

The molecular and cellular mechanisms that allow adult-stage neurons to regenerate following damage are poorly understood. Recently, axons of motoneurons and mechanosensory neurons in adult C. elegans were found to regrow after being snipped by femtosecond laser ablation. Here, we explore the molecular determinants of adult-stage axon regeneration using the AVM mechanosensory neurons. The first step in AVM axon development is a pioneer axonal projection from the cell body to the ventral nerve cord. We show that regeneration of the AVM axon to the ventral nerve cord lacks the deterministic precision of initial axon development, requiring competition and pruning of unwanted axon branches. Nevertheless, axons of injured AVM neurons regrow to the ventral nerve cord with over 60% reliability in adult animals. In addition, in contrast to initial development, axon guidance during regeneration becomes heavily dependent on cytoplasmic protein MIG-10/Lamellipodin but independent of UNC-129/TGF-β repellent and UNC-40/DCC receptor, and axon growth during regeneration becomes heavily dependent on UNC-34/Ena and CED-10/Rac actin regulators. Thus, C. elegans may be used as a genetic system to characterize novel cellular and molecular mechanisms underlying adult-stage nervous system regeneration.

Key words: C. elegans, Femtosecond laser axotomy, Regeneration

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