Phosphorylation-dependent differential regulation of plant growth, cell death, and innate immunity by the regulatory receptor-like kinase BAK1.
Phosphorylation-dependent differential regulation of plant growth, cell death, and innate immunity by the regulatory receptor-like kinase BAK1.
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DOI：
10.1371/journal.pgen.1002046
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发表时间：
2011-04
期刊：
影响因子：
4.5
通讯作者：
Zipfel C
中科院分区：
文献类型：
--
作者：
Schwessinger B;Roux M;Kadota Y;Ntoukakis V;Sklenar J;Jones A;Zipfel C
植物严重依赖类受体激酶（RLK）来感知和整合外部和内部刺激。拟南芥调节性富含亮氨酸重复序列 RLK (LRR-RLK) BAK1 参与类固醇激素反应、先天免疫和细胞死亡控制。在这里，我们描述了 BAK1 的一个新等位基因 bak1-5 对三种不同的 BAK1 依赖性信号通路的差异调节。由 BAK1 依赖性 RK FLS2 和 EFR 介导的先天免疫信号在 bak1-5 突变植物中受到严重损害。然而，bak1-5 突变体的 BR 信号传导或细胞死亡控制并未受损。我们还表明，与 RD 激酶 BRI1 相比，非 RD 激酶 FLS2 和 EFR 具有非常低的激酶活性，并且我们表明两者都不能在体外转磷酸化 BAK1。此外，所有伙伴的激酶活性对于配体诱导的 FLS2 或 EFR 与植物中 BAK1 的异聚化是完全可有可无的，揭示了另一种途径特异性机制差异。 bak1-5 中 FLS2 和 EFR 依赖性信号传导的特异性抑制并非由于 BAK1-5 与相应配体结合 RK 的差异相互作用，而是需要 BAK1-5 激酶活性。总的来说，我们的结果证明了RLK BAK1对植物生长、先天免疫和细胞死亡的磷酸化依赖性差异控制，这可能揭示了配体结合RD和非RD RK调节的分子机制的关键差异。植物需要适应不断变化的环境才能生存。跨膜受体激酶对于将细胞外刺激转化为细胞内反应至关重要。一个关键问题是植物如何保持信号特异性以应对多种胁迫和内源激素。类固醇激素诱导的生长反应和识别保守微生物分子引发的先天免疫取决于常见的调节受体样激酶 BAK1，该激酶也参与细胞死亡控制。目前尚不清楚 BAK1 是否提供信号传导特异性，或者它是否仅仅是信号传导增强剂。在这里，我们描述了新的蛋白质变体 BAK1-5，它特异性地阻断先天免疫反应，而不影响类固醇反应或细胞死亡。这明确地表明 BAK1 在植物信号传导中的作用可以在机械上分开。重要的是，免疫信号传导受损并不是由 BAK1-5 与免疫受体相互作用丧失引起的，而是由于激酶活性改变所致。因此，BAK1 依赖性信号通路受到不同的磷酸化依赖性调节。对 BAK1 的这种新型突变体版本的检查将能够详细研究 BAK1 在植物先天免疫中的机制作用，而且更广泛地还将为植物跨膜受体信号传导特异性提供宝贵的见解。
Plants rely heavily on receptor-like kinases (RLKs) for perception and integration of external and internal stimuli. The Arabidopsis regulatory leucine-rich repeat RLK (LRR-RLK) BAK1 is involved in steroid hormone responses, innate immunity, and cell death control. Here, we describe the differential regulation of three different BAK1-dependent signaling pathways by a novel allele of BAK1, bak1-5. Innate immune signaling mediated by the BAK1-dependent RKs FLS2 and EFR is severely compromised in bak1-5 mutant plants. However, bak1-5 mutants are not impaired in BR signaling or cell death control. We also show that, in contrast to the RD kinase BRI1, the non-RD kinases FLS2 and EFR have very low kinase activity, and we show that neither was able to trans-phosphorylate BAK1 in vitro. Furthermore, kinase activity for all partners is completely dispensable for the ligand-induced heteromerization of FLS2 or EFR with BAK1 in planta, revealing another pathway specific mechanistic difference. The specific suppression of FLS2- and EFR-dependent signaling in bak1-5 is not due to a differential interaction of BAK1-5 with the respective ligand-binding RK but requires BAK1-5 kinase activity. Overall our results demonstrate a phosphorylation-dependent differential control of plant growth, innate immunity, and cell death by the regulatory RLK BAK1, which may reveal key differences in the molecular mechanisms underlying the regulation of ligand-binding RD and non-RD RKs. Plants need to adapt to their ever-changing environment for survival. Transmembrane receptor kinases are essential to translate extracellular stimuli into intracellular responses. A key question is how plants maintain signaling specificity in response to multiple stresses and endogenous hormones. Growth responses induced by steroid hormones and innate immunity triggered by recognition of conserved microbial molecules depend on the common regulatory receptor-like kinase BAK1, which is also involved in cell death control. It is still unclear if BAK1 provides signaling specificity or if it is a mere signaling enhancer. Here, we describe the novel protein variant BAK1-5 that specifically blocks innate immune responses without affecting steroid responses or cell death. This unambiguously demonstrates that the role of BAK1 in plant signaling can be mechanistically separated. Importantly, the impairment of immune signaling is not caused by a loss of interaction of BAK1-5 with immune receptors but is due to an altered kinase activity. Thus, BAK1-dependent signaling pathways are under a differential phosphorylation-dependent regulation. The examination of this novel mutant version of BAK1 will enable detailed studies into the mechanistic role of BAK1 in plant innate immunity, but also more generally will provide invaluable insights into transmembrane receptor signaling specificity in plants.
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