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首页> 美国卫生研究院文献>The Journal of Biological Chemistry >Arabidopsis thaliana rapid alkalinization factor 1–mediated root growth inhibition is dependent on calmodulin-like protein 38
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Arabidopsis thaliana rapid alkalinization factor 1–mediated root growth inhibition is dependent on calmodulin-like protein 38

机译：拟南芥快速碱化因子1介导的根生长抑制依赖于钙调蛋白样蛋白38

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Arabidopsis thaliana rapid alkalinization factor 1 (AtRALF1) is a small secreted peptide hormone that inhibits root growth by repressing cell expansion. Although it is known that AtRALF1 binds the plasma membrane receptor FERONIA and conveys its signals via phosphorylation, the AtRALF1 signaling pathway is largely unknown. Here, using a yeast two-hybrid system to search for AtRALF1-interacting proteins in Arabidopsis, we identified calmodulin-like protein 38 (CML38) as an AtRALF1-interacting partner. We also found that CML38 and AtRALF1 are both secreted proteins that physically interact in a Ca2+- and pH-dependent manner. CML38-knockout mutants generated via T-DNA insertion were insensitive to AtRALF1, and simultaneous treatment with both AtRALF1 and CML38 proteins restored sensitivity in these mutants. Hybrid plants lacking CML38 and having high accumulation of the AtRALF1 peptide did not exhibit the characteristic short-root phenotype caused by AtRALF1 overexpression. Although CML38 was essential for AtRALF1-mediated root inhibition, it appeared not to have an effect on the AtRALF1-induced alkalinization response. Moreover, acridinium-labeling of AtRALF1 indicated that the binding of AtRALF1 to intact roots is CML38-dependent. In summary, we describe a new component of the AtRALF1 response pathway. The new component is a calmodulin-like protein that binds AtRALF1, is essential for root growth inhibition, and has no role in AtRALF1 alkalinization.
机译：拟南芥快速碱化因子1（AtRALF1）是一种小分子分泌的肽激素，可通过抑制细胞膨胀来抑制根的生长。尽管已知AtRALF1结合质膜受体FERONIA并通过磷酸化传递其信号，但很大程度上未知AtRALF1信号传导途径。在这里，使用酵母双杂交系统在拟南芥中搜索与AtRALF1相互作用的蛋白，我们确定了钙调蛋白样蛋白38（CML38）为与AtRALF1相互作用的伴侣。我们还发现CML38和AtRALF1都是以Ca 2 + -和pH依赖的方式发生物理相互作用的分泌蛋白。通过T-DNA插入产生的CML38基因敲除突变体对AtRALF1不敏感，同时用AtRALF1和CML38蛋白同时处理恢复了这些突变体的敏感性。缺少CML38且具有高积累的AtRALF1肽的杂种植物没有表现出由AtRALF1过表达引起的特征性短根表型。尽管CML38对于AtRALF1介导的根抑制至关重要，但它似乎对AtRALF1诱导的碱化反应没有影响。此外，AtRALF1的a啶标记表明AtRALF1与完整根的结合是CML38依赖性的。总之，我们描述了AtRALF1反应途径的新组成部分。新的成分是一种钙调蛋白样蛋白，它与AtRALF1结合，对于抑制根生长至关重要，并且在AtRALF1碱化中没有作用。

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