A receptor-like protein mediates the response to pectin modification by activating brassinosteroid signaling-猫眼课题宝

DOI：

10.1073/pnas.1322979111

发表时间：

2014-10

期刊：

Proceedings of the National Academy of Sciences

影响因子：

通讯作者：

中科院分区：

其他

文献类型：

作者：

Sebastian Wolf;Dieuwertje Van der Does;Friederike Ladwig;C. Sticht;A. Kolbeck;Ann-Kathrin Schürholz;Sebastian Augustin;Nana F. Keinath;T. Rausch;S. Greiner;K. Schumacher;K. Harter;C. Zipfel;H. Höfte

植物的生长发育依赖于细胞壁的生物合成和重塑。为了协调这两个过程，监视机制已经发展到监测细胞壁的状态。油菜素类固醇（BR）激素信号通路在生长控制中起着重要作用，并调节大量细胞壁相关基因的表达。我们以前已经表明，来自细胞壁的反馈信号可以调节BR通路的输出，确保细胞壁的稳态和完整性。在这里，我们确定了受体样蛋白（RLP 44），它介导的BR信号通过直接与BR辅助受体BAK 1的相互作用的激活。因此，RLP 44将细胞壁监视与激素信号传导整合以控制细胞壁完整性和生长。油菜素类固醇（BR）信号转导模块是植物形态建成的重要调控因子，大量的BR响应细胞壁相关基因和BR突变体严重的生长缺陷表明了这一点。尽管对信号成分有详细的了解，但对这种自分泌/旁分泌信号模块在生长控制中的逻辑仍然知之甚少。最近，广泛的串扰与其他信号通路已被证明，表明BR信号的输出，如基因表达的变化，受到复杂的控制机制。我们以前提供的证据BR信号在控制细胞壁完整性的反馈回路中的作用。在这里，我们确定了这个反馈回路的第一个专门的组成部分：受体样蛋白（RLP 44），这是必不可少的补偿触发BR信号后，在细胞壁中的果胶脱甲酯化的抑制。RLP 44是正常生长和应激反应所必需的，并与BR信号传导途径连接，推测是通过与调节受体样激酶BAK 1的直接相互作用。这些发现证实了BR在控制反馈信号模块的敏感性中的作用，所述反馈信号模块参与在细胞扩增期间维持细胞壁的物理化学稳态。

Significance Plant growth and development depend on the biosynthesis and remodeling of the cell wall. To coordinate these two processes, surveillance mechanisms have evolved to monitor the state of the cell wall. The brassinosteroid (BR) hormone signaling pathway plays an essential role in growth control and regulates the expression of a plethora of cell wall-related genes. We have previously shown that feedback signaling from the wall can modulate the outputs of the BR pathway, ensuring cell wall homeostasis and integrity. Here, we identified a receptor-like protein (RLP44), which mediates the activation of BR signaling through direct interaction with the BR coreceptor BAK1. Thus, RLP44 integrates cell wall surveillance with hormone signaling to control cell wall integrity and growth. The brassinosteroid (BR) signaling module is a central regulator of plant morphogenesis, as indicated by the large number of BR-responsive cell wall-related genes and the severe growth defects of BR mutants. Despite a detailed knowledge of the signaling components, the logic of this auto-/paracrine signaling module in growth control remains poorly understood. Recently, extensive cross-talk with other signaling pathways has been shown, suggesting that the outputs of BR signaling, such as gene-expression changes, are subject to complex control mechanisms. We previously provided evidence for a role of BR signaling in a feedback loop controlling the integrity of the cell wall. Here, we identify the first dedicated component of this feedback loop: a receptor-like protein (RLP44), which is essential for the compensatory triggering of BR signaling upon inhibition of pectin de-methylesterification in the cell wall. RLP44 is required for normal growth and stress responses and connects with the BR signaling pathway, presumably through a direct interaction with the regulatory receptor-like kinase BAK1. These findings corroborate a role for BR in controlling the sensitivity of a feedback signaling module involved in maintaining the physico-chemical homeostasis of the cell wall during cell expansion.

A receptor-like protein mediates the response to pectin modification by activating brassinosteroid signaling

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