The CaMKII UNC-43 activates the MAPKKK NSY-1 to execute a lateral signaling decision required for asymmetric olfactory neuron fates
The CaMKII UNC-43 activates the MAPKKK NSY-1 to execute a lateral signaling decision required for asymmetric olfactory neuron fates
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DOI：
10.1016/s0092-8674(01)00313-0
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发表时间：
2001-04-20
期刊：
影响因子：
64.5
通讯作者：
Bargmann, CI
中科院分区：
文献类型：
--
作者：
Sagasti, A;Hisamoto, N;Bargmann, CI
由轴突接触和钙信号介导的随机细胞命运决定导致两个双边对称的AWC神经元之一AWCL或AWCR表达候选嗅觉受体str-2， nsy-1突变体在两个神经元中表达str-2，破坏AWC的不对称性，nsy-1编码人类MAP激酶激酶激酶（MAPKKK） ASK1的同源物，这是JNK和p38激酶的激活剂。基于遗传上位性分析，nsy-1似乎作用于CaMKII unc-43的下游，并且nsy-1与unc-43相关，这表明unc-43 /CaMKII激活了nsy-1 MAP激酶盒。马赛克分析表明，UNC-43和NSY-1主要在细胞自主执行步骤中起作用，抑制一个AWC细胞中str-2的表达，这是协调两个细胞命运的初始侧信号通路的下游。
A stochastic cell fate decision mediated by axon contact and calcium signaling causes one of the two bilaterally symmetric AWC neurons, either AWCL or AWCR, to express the candidate olfactory receptor str-2 nsy-1 mutants express str-2 in both neurons, disrupting AWC asymmetry, nsy-1 encodes a homolog of the human MAP kinase kinase kinase (MAPKKK) ASK1, an activator of JNK and p38 kinases. Based on genetic epistasis analysis, nsy-1 appears to act downstream of the CaMKII unc-43, and NSY-1 associates with UNC-43, suggesting that UNC-43/CaMKII activates the NSY-1 MAP kinase cassette. Mosaic analysis demonstrates that UNC-43 and NSY-1 act primarily in a cell-autonomous execution step that represses str-2 expression in one AWC cell, downstream of the initial lateral signaling pathway that coordinates the fates of the two cells.