Receptor tyrosine phosphatase CLR-1 acts in skin cells to promote sensory dendrite outgrowth.

Receptor tyrosine phosphatase CLR-1 acts in skin cells to promote sensory dendrite outgrowth.
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受体酪氨酸磷酸酶 CLR-1 在皮肤细胞中发挥作用,促进感觉树突生长。

DOI:
10.1016/j.ydbio.2016.03.001
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发表时间:
2016-05-01
影响因子:
2.7
通讯作者:
Shen K
Shen K
中科院分区:
生物学3区
文献类型:
--
作者:
Liu X;Wang X;Shen K

文献摘要

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感觉树突的形态发生受内在和外在因素的指导。细胞外环境在树突生长和分枝的模式中起着指导性的作用。然而,其分子机制还不清楚。在秀丽隐杆线虫中,本体感受神经元PVD在皮下组织附近形成高度分支的感觉树突。我们报道了受体酪氨酸磷酸酶Ⅶ-1在皮下组织中的功能,以形成PVD树突状分支。clr-1基因突变导致第四分支缺失,二级分支减少,异位分支增加。α-l对枝晶的生长是必需的,但对丝状伪足的形成则不是必需的。它的作用依赖于细胞内磷酸酶结构域,而不是细胞外粘附结构域,表明它通过去磷酸化下游因子而不是通过与神经元的直接粘附发挥作用。遗传分析显示clr-1也与SAX-7/DMA-1通路平行地控制PVD初生树突发育。我们提供了一个新的环境因素PVD枝晶形态发生的证据。
Sensory dendrite morphogenesis is directed by intrinsic and extrinsic factors. The extracellular environment plays instructive roles in patterning dendrite growth and branching. However, the molecular mechanism is not well understood. In Caenorhabditis elegans, the proprioceptive neuron PVD forms highly branched sensory dendrites adjacent to the hypodermis. We report that receptor tyrosine phosphatase CLR-1 functions in the hypodermis to pattern the PVD dendritic branches. Mutations in clr-1 lead to loss of quaternary branches, reduced secondary branches and increased ectopic branches. CLR-1 is necessary for the dendrite extension but not for the initial filopodia formation. Its role is dependent on the intracellular phosphatase domain but not the extracellular adhesion domain, indicating that it functions through dephosphorylating downstream factors but not through direct adhesion with neurons. Genetic analysis reveals that clr-1 also functions in parallel with SAX-7/DMA-1 pathway to control PVD primary dendrite development. We provide evidence of a new environmental factor for PVD dendrite morphogenesis.