Mitogen-activated protein kinase 6 negatively regulates secondary wall biosynthesis by modulating MYB46 protein stability in Arabidopsis thaliana.
Mitogen-activated protein kinase 6 negatively regulates secondary wall biosynthesis by modulating MYB46 protein stability in Arabidopsis thaliana.
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DOI：
10.1371/journal.pgen.1009510
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发表时间：
2021-04
期刊：
影响因子：
4.5
通讯作者：
Han KH
中科院分区：
文献类型：
--
作者：
Im JH;Ko JH;Kim WC;Crain B;Keathley D;Han KH
R2R3-MYB 转录因子 MYB46 充当次生细胞壁生物合成的主开关，确保次生壁生物合成基因在次生壁对生长和发育至关重要的组织中精确表达。同时，当/当不希望形成次生壁时，需要抑制其功能。人们对于如何实现这种对次生细胞壁形成的相反控制知之甚少。我们使用 MYB46 和丝裂原激活蛋白激酶 6 (MPK6) 的瞬时和转基因表达来研究 MYB46 翻译后调控的分子机制。我们发现 MYB46 被 MPK6 磷酸化，导致 MYB46 通过泛素介导的蛋白酶体途径发生位点特异性磷酸化依赖性降解。此外，还发现 MPK6 介导的 MYB46 磷酸化可调节 MYB46 的植物次生壁形成功能。此外，我们提供的实验证据表明，MYB83（MYB46 的旁系同源物）不受 MPK6 调节。 MPK 信号传导与 MYB46 功能的耦合提供了对 MYB46 对次生壁生物合成的组织和/或条件特异性活性的深入了解。次生细胞壁对于植物生长至关重要，并且作为纤维、纸浆和可再生能源对人类具有经济重要性。次生壁生物合成的主开关 MYB46 可确保次生壁至关重要的组织中生物合成基因的精确表达。然而，在环境胁迫引发的营养生长暂时停止期间，需要抑制次生壁的形成。尽管 MYB46 的表达因非生物胁迫而上调，但次生壁的形成可能不会发生。这种相反的控制是如何实现的呢？丝裂原激活蛋白激酶（MPK）级联是真核生物中最保守的信号转导系统之一，在调节与环境刺激和植物激素相关的生化和生理变化中发挥着至关重要的作用。在本报告中，我们表明 MYB46 在盐胁迫期间受到 MPK6 的负向调节，为植物将环境信号纳入次生壁生物合成差异调节的机制提供了新的见解。
The R2R3-MYB transcription factor MYB46 functions as a master switch for secondary cell wall biosynthesis, ensuring the exquisite expression of the secondary wall biosynthetic genes in the tissues where secondary walls are critical for growth and development. At the same time, suppression of its function is needed when/where formation of secondary walls is not desirable. Little is known about how this opposing control of secondary cell wall formation is achieved. We used both transient and transgenic expression of MYB46 and mitogen-activated protein kinase 6 (MPK6) to investigate the molecular mechanism of the post-translational regulation of MYB46. We show that MYB46 is phosphorylated by MPK6, leading to site specific phosphorylation-dependent degradation of MYB46 by the ubiquitin-mediated proteasome pathway. In addition, the MPK6-mediated MYB46 phosphorylation was found to regulate in planta secondary wall forming function of MYB46. Furthermore, we provide experimental evidences that MYB83, a paralog of MYB46, is not regulated by MPK6. The coupling of MPK signaling to MYB46 function provides insights into the tissue- and/or condition-specific activity of MYB46 for secondary wall biosynthesis. Secondary cell walls are critical for plant growth and of economic importance to humans as fiber, pulp for paper, and as a renewable source of energy. A master switch for secondary wall biosynthesis, MYB46, ensures the exquisite expression of the biosynthetic genes in the tissues where secondary walls are critical. However, suppression of secondary wall formation is needed during impermanent cessation of vegetative growth triggered by environmental stresses. Although the expression of MYB46 is upregulated by abiotic stresses, secondary wall formation may not occur. How is this opposing control achieved? The mitogen-activated protein kinase (MPK) cascade is among the most conserved signal transduction systems in eukaryotes and plays a crucial role in the regulation of biochemical and physiological changes associated with environmental stimuli and phytohormones. In this report, we show that MYB46 is negatively regulated by MPK6 during salt stress, providing a novel insight into a mechanism by which plants incorporate environmental signals into differential regulation of secondary wall biosynthesis.
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