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The Dictyostelium MAPK ERK1 is phosphorylated in a secondary response to early developmental signaling

机译：Dictyostelium MAPK ERK1在早期发育信号的次级反应中被磷酸化

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Previous reports have suggested that the two mitogen-activated protein kinases (MAPKs) in Dictyostelium discoideum, ERK1 and ERK2, can be directly activated in response to external cAMP even though these MAPKs play different roles in the developmental life cycle. To better characterize MAPK regulation, the levels of phosphorylated MAPKs were analyzed in response to external signals. Only ERK2 was rapidly phosphorylated in response to the chemoattractants, cAMP and folate. In contrast, the phosphorylation of ERK1 occurred as a secondary or indirect response to these stimuli and this phosphorylation was enhanced by cell-cell interactions, suggesting that other external signals can activate ERK1. The phosphorylation of ERK1 or ERK2 did not require the function of the other MAPK in these responses. Folate stimulation of a chimeric population of erk1(-) and g alpha 4(-) cells revealed that the phosphorylation of ERK1 could be mediated through an intercellular signal other than folate. Loss of ERK1 function suppressed the developmental delay and the deficiency in anterior cell localization associated with g alpha 5(-) mutants suggesting that ERK1 function can be down regulated through G alpha 5 subunit-mediated signaling. However, no major changes in the phosphorylation of ERK1 were observed in g alpha 5(-) cells suggesting that the G alpha 5 subunit signaling pathway does not regulate the phosphorylation of ERK1. These findings suggest that the activation of ERK1 occurs as a secondary response to chemoattractants and that other cell-cell signaling mechanisms contribute to this activation. Ga5 subunit signaling can down regulate ERK1 function to promote prestalk cell development but not through major changes to the level of phosphorylated ERK1. (C) 2014 Elsevier Inc. All rights reserved.
机译：先前的报告表明，盘基网柄菌中的两种促分裂原活化蛋白激酶（MAPK）ERK1和ERK2可以直接响应外部cAMP而被激活，即使这些MAPK在发育生命周期中发挥不同的作用。为了更好地表征MAPK调节，响应外部信号分析了磷酸化MAPK的水平。仅ERK2响应化学吸引剂，cAMP和叶酸而迅速磷酸化。相反，ERK1的磷酸化是对这些刺激的继发性或间接反应，并且这种磷酸化通过细胞间相互作用而增强，表明其他外部信号也可以激活ERK1。在这些反应中，ERK1或ERK2的磷酸化不需要其他MAPK的功能。叶酸刺激erk1（-）和g alpha 4（-）细胞的嵌合群体揭示ERK1的磷酸化可能是通过叶酸以外的其他细胞间信号介导的。 ERK1功能的丧失抑制了发育延迟和与g alpha 5（-）突变体相关的前细胞定位不足，这表明ERK1功能可以通过G alpha 5亚基介导的信号传导而下调。但是，在g alpha 5（-）细胞中未观察到ERK1磷酸化的重大变化，这表明G alpha 5亚基信号传导途径不能调节ERK1的磷酸化。这些发现表明，ERK1的激活是对化学引诱剂的继发反应，其他细胞信号机制也参与了这种激活。 Ga5亚基信号传导可以下调ERK1功能，以促进茎前细胞发育，但不能通过磷酸化ERK1水平的重大变化来实现。 （C）2014 Elsevier Inc.保留所有权利。

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