首页> 外文期刊>Developmental dynamics: an official publication of the American Association of Anatomists >ENU-3 functions in an UNC-6etrin dependent pathway parallel to UNC-40/DCC/frazzled for outgrowth and guidance of the touch receptor neurons in C. elegans
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ENU-3 functions in an UNC-6etrin dependent pathway parallel to UNC-40/DCC/frazzled for outgrowth and guidance of the touch receptor neurons in C. elegans

机译:ENU-3在UNC-6 / netrin依赖性途径中起作用,与UNC-40 / DCC /发皱的平行,用于秀丽隐杆线虫的接触受体神经元的长出和引导。

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摘要

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. Developmental Dynamics 243:459-467, 2014.
机译:背景:UNC-6和SLT-1指导AVM和PVM触摸受体神经元的腹侧定向过程的迁移,UNC-6指导秀丽隐杆线虫运动神经元的DA和DB类轴突。 UNC-6受体是UNC-5和UNC-40。在缺少UNC-5的情况下,一部分DB运动神经元的轴突生长缺陷会因enu-3中的突变而增强。结果:enu-3突变增强了AVM和PVM触摸受体神经元的腹侧引导,远端尖端细胞的背侧引导中的缺陷,并导致UNC-6突变株中UNC-6的轴突出现了其他结构缺陷。依赖方式。这些观察结果表明,ENU-3和UNC-40在依赖于UNC-6的平行途径中起作用。 ENU-3完全依赖于UNC-40来发挥其对运动神经元轴突生长的完全作用。结论:ENU-3在AVM和PVM的腹侧引导以及远端尖端细胞的背侧引导中以与UNC-40平行的UNC-6依赖性途径起作用。运动神经元轴突生长缺陷是由UNC-40的存在和功能性UNC-5或UNC-6的缺乏引起的,而缺陷则由功能性ENU-3的缺乏增强。发展动态243:459-467,2014。

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