Mutations of the AtYAK1 Kinase Suppress TOR Deficiency in Arabidopsis
Mutations of the AtYAK1 Kinase Suppress TOR Deficiency in Arabidopsis
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DOI：
10.1016/j.celrep.2019.05.074
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发表时间：
2019-06-18
期刊：
影响因子：
8.8
通讯作者：
Meyer, Christian
中科院分区：
文献类型：
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作者：
Forzani, Celine;Duarte, Gustavo T.;Meyer, Christian
雷帕霉素(TOR)激酶的靶标是一种保守的能量感受器，它调节生长对环境提示的反应。然而，对植物中的TOR信号通路知之甚少。我们使用了受SEC13蛋白8(LST8-1)基因影响的拟南芥品系，LST8-1是TOR复合体的核心元件，以寻找抑制突变。分离到两个生长改善的抑制株，它们携带编码双特异性酪氨酸磷酸化调节激酶(Dyrk)家族成员的另一种激酶1(AtYAK1)基因的突变。Atyak1突变部分挽救了Ist8-1-1突变体的发育缺陷，并使其对TOR抑制剂AZD-8055产生了抗性。此外，atyak1突变抑制了Ist8-1-1突变体的转录和代谢扰动以及脱落酸(ABA)过敏性。AtYAK1与TOR复合体的一个成分TOR(Raptor)的调节相关蛋白相互作用，并被TOR磷酸化。因此，我们的发现表明，AtYAK1是一种TOR效应器，可能需要关闭才能激活植物生长。
The target of rapamycin (TOR) kinase is a conserved energy sensor that regulates growth in response to environmental cues. However, little is known about the TOR signaling pathway in plants. We used Arabidopsis lines affected in the lethal with SEC13 protein 8 (LST8-1) gene, a core element of the TOR complex, to search for suppressor mutations. Two suppressor lines with improved growth were isolated that carried mutations in the Yet Another Kinase 1 (AtYAK1) gene encoding a member of the dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) family. Atyakl mutations partly rescued the developmental defects of Ist8-1-1 mutants and conferred resistance to the TOR inhibitor AZD-8055. Moreover, atyakl mutations suppressed the transcriptomic and metabolic perturbations as well as the abscisic acid (ABA) hypersensitivity of the Ist8-1-1 mutants. AtYAK1 interacted with the regulatory-associated protein of TOR (RAPTOR), a component of the TOR complex, and was phosphorylated by TOR. Thus, our findings reveal that AtYAK1 is a TOR effector that probably needs to be switched off to activate plant growth.