Genetic screen for genes affecting axon regeneration in C. elegans

University Of Utah, Salt Lake City UT

Investigators

Abstract

Brain and spinal cord neurons in mammals, including humans, do not regenerate when they are broken due to injury or disease. Yet, neurons have a tremendous capacity for regeneration in mammalian embryos and in some adult animals. The puzzle of why adult mammalian neurons lose their capacity to regenerate can be solved by using the simple model organism, C. elegans. A genetic mutation was discovered in C. elegans that causes axons to break spontaneously. In response to these spontaneous axon breaks, the neurons successfully regrow new axons back to their target muscles. This spontaneous axon break, followed by axon regeneration, will be used to test the function of each gene in the C. elegans genome for its effect on axon regeneration. This would be the first genetic screen to identify all genes involved in axon regeneration in any organism and should lead to a comprehensive and fundamental understanding of the signaling pathways controlling axon regeneration. It should also allow identification of the signaling changes that occur with age that prevent axon regeneration in most adult mammalian neurons. The similarity between genes in C. elegans and humans means that any knowledge gained from the screen should be applicable to human nerve cell regeneration and provide rational targets for new drug therapies. This research will also provide training in cutting edge research technologies for graduate students and undergraduates, and will provide research opportunities for high school students through the University of Utah Bio-Sciences program that places students in laboratories for 7 weeks each summer.