Literature DB >> 24123761

ENU-3 functions in an UNC-6/netrin dependent pathway parallel to UNC-40/DCC/frazzled for outgrowth and guidance of the touch receptor neurons in C. elegans.

Callista Yee1, Roxana Florica, Jeffrey Fillingham, Marie T Killeen.   

Abstract

BACKGROUND: UNC-6 and SLT-1 guide the migrations of the ventrally directed processes of the AVM and PVM touch receptor neurons and UNC-6 guides the axons of the DA and DB classes of motor neurons in C. elegans. The UNC-6 receptors are UNC-5 and UNC-40. The axon outgrowth defects of a subset of the DB motor neurons in the absence of UNC-5 are enhanced by mutations in enu-3.
RESULTS: An enu-3 mutation enhances defects in ventral guidance of the processes of the AVM and PVM touch receptor neurons, the dorsal guidance of the distal tip cell and causes additional architectural defects in axons in unc-40 mutant strains in an UNC-6 dependent manner. These observations suggest that ENU-3 and UNC-40 function in parallel pathways dependent on UNC-6. ENU-3 depends on the presence of UNC-40 for its full effect on motor neuron axon outgrowth.
CONCLUSIONS: ENU-3 works in an UNC-6 dependent pathway parallel to UNC-40 in ventral guidance of AVM and PVM and in dorsal guidance of the distal tip cells. Motor neuron axon outgrowth defects are caused by the presence of UNC-40 and the absence of functional UNC-5 or UNC-6 and defects are enhanced by the absence of functional ENU-3.
Copyright © 2013 Wiley Periodicals, Inc.

Entities:  

Keywords:  AVM; DA and DB motor neuron axon outgrowth; ENU-3; UNC-40/DCC; UNC-5; UNC-6/Netrin

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Year:  2013        PMID: 24123761     DOI: 10.1002/dvdy.24063

Source DB:  PubMed          Journal:  Dev Dyn        ISSN: 1058-8388            Impact factor:   3.780


  1 in total

1.  SYD-1C, UNC-40 (DCC) and SAX-3 (Robo) function interdependently to promote axon guidance by regulating the MIG-2 GTPase.

Authors:  Yan Xu; Hidenori Taru; Yishi Jin; Christopher C Quinn
Journal:  PLoS Genet       Date:  2015-04-15       Impact factor: 5.917

  1 in total

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