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Mitogen-Activated Protein Kinase Regulated by the CLAVATA Receptors Contributes to Shoot Apical Meristem Homeostasis

机译:由CLAVATA受体调节的丝裂原激活的蛋白激酶有助于拍摄顶端的分生组织稳态。

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In Arabidopsis, the CLAVATA (CLV) pathway operates in the regulation of the size of the stem cell population in the shoot apical meristem (SAM). CLV3 functions as a small peptide ligand to negatively regulate the expression of the WUSCHEL (WUS) transcription factor through three major receptor kinase complexes of CLV1, CLV2-SUPPRESSOR OF LLP1-2 (SOL2)/CORYNE (CRN) and recently identified RECEPTOR-LIKE PROTEIN KINASE 2 (RPK2)/TOADSTOOL 2 (TOAD2). Aiming to understand the precise molecular details of CLV3 signaling, we investigated the contribution of phospho-signaling, potentially regulated by these kinase complexes, to the CLV pathway. We detected CLV3-triggered CLV1 phosphorylation, which is also conditioned by the rest of the CLV receptors, presumably by their direct association. Our comprehensive analysis of the activities of the respective CLV receptors on mitogen-activated protein kinases (MAPKs) suggested that the precise balanced regulation of MAPK activity by the CLV receptors is likely to be key for SAM homeostasis.
机译:在拟南芥中,CLAVATA(CLV)途径可调控芽尖分生组织(SAM)中干细胞种群的大小。 CLV3可作为一种小的肽配体,通过CLV1,CLP2-LLP1-2的抑制因子(SOL2)/ CORYNE(CRN)和最近发现的RECEPTOR-LIKE的三种主要受体激酶复合物负调控WUSCHEL(WUS)转录因子的表达蛋白质激酶2(RPK2)/ TOADSTOOL 2(TOAD2)。为了了解CLV3信号传导的精确分子细节,我们研究了可能由这些激酶复合物调节的磷酸信号对CLV通路的贡献。我们检测到CLV3触发的CLV1磷酸化,这也受其他CLV受体(可能是它们的直接缔合)的调节。我们对各个CLV受体在丝裂原活化蛋白激酶(MAPK)上的活性的全面分析表明,CLV受体对MAPK活性的精确平衡调节可能是SAM稳态的关键。

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