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Novel Caenorhabditis elegans unc‐119 axon outgrowth defects correlate with behavioral phenotypes that are partially rescued by nonneural unc‐119
Author(s) -
Materi Wayne,
Pilgrim David
Publication year - 2005
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.20130
Subject(s) - caenorhabditis elegans , biology , axon , ventral nerve cord , microbiology and biotechnology , nervous system , phenotype , neuroscience , anatomy , genetics , gene
UNC‐119 function is necessary for the correct development of the Caenorhabditis elegans nervous system. Worms mutant for unc‐119 exhibit nervous system structural defects, including supernumerary axon branches, defasciculated nerve fibers, and choice point errors. Axons of both mechanosensory (ALM) and chemo‐ sensory (ASI) neurons have elongation defects within the nerve ring. Expressing unc‐119 cDNA in mechanosensory neurons rescues the elongation defect of ALM axons, but expression in ASI neurons does not rescue ASI axon elongation defects. Neither gross movement nor dauer larva formation defects are rescued in either case. However, expressing a construct including introns under the control of the same promoters results in substantial rescue of phenotypic defects. In these cases reporter expression expands to tissues outside those specified by the promoter, notably into head muscles. Surprisingly, expressing an unc‐119 cDNA construct under the control of a muscle‐specific promoter fully rescues the dauer formation defect and substantially rescues movement. Thus, although UNC‐119 normally acts in a cell‐autonomous fashion, the cell‐nonautonomous rescue of neural function suggests that it either acts at the cell surface or that it can be transported into the cell from the extracellular environment and play its normal role. genesis 42:104–116, 2005. © 2005 Wiley‐Liss, Inc.