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ENU-3在与UNC-40/DCC/卷曲蛋白平行的UNC-6/网蛋白依赖途径中发挥作用,以促进秀丽隐杆线虫触觉感受神经元的生长和导向。

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.

作者信息

Yee Callista, Florica Roxana, Fillingham Jeffrey, Killeen Marie T

机构信息

Graduate Program in Molecular Science, Ryerson University, Toronto, Ontario, Canada M5B 2K3.

出版信息

Dev Dyn. 2014 Mar;243(3):459-67. doi: 10.1002/dvdy.24063. Epub 2013 Dec 25.

DOI:10.1002/dvdy.24063
PMID:24123761
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.

摘要

背景

UNC-6和SLT-1引导秀丽隐杆线虫中AVM和PVM触觉受体神经元腹侧定向突起的迁移,UNC-6引导DA和DB类运动神经元的轴突。UNC-6受体是UNC-5和UNC-40。在缺乏UNC-5的情况下,DB运动神经元亚群的轴突生长缺陷会因enu-3突变而加剧。

结果

enu-3突变以UNC-6依赖的方式加剧了AVM和PVM触觉受体神经元突起腹侧引导的缺陷、远端末梢细胞背侧引导的缺陷,并在unc-40突变株的轴突中导致额外的结构缺陷。这些观察结果表明,ENU-3和UNC-40在依赖UNC-6的平行途径中发挥作用。ENU-3对运动神经元轴突生长的全面影响依赖于UNC-40的存在。

结论

在AVM和PVM的腹侧引导以及远端末梢细胞的背侧引导中,ENU-3在与UNC-40平行的UNC-6依赖途径中起作用。运动神经元轴突生长缺陷是由UNC-40的存在以及功能性UNC-5或UNC-6的缺失引起的,而功能性ENU-3的缺失会加剧这些缺陷。

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