Degradation of the ABA co-receptor ABI1 by PUB12/13 U-box E3 ligases.
Degradation of the ABA co-receptor ABI1 by PUB12/13 U-box E3 ligases.
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PUB12/13 U-box E3 连接酶降解 ABA 辅助受体 ABI1。
DOI：
10.1038/ncomms9630
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发表时间：
2015-10-20
影响因子：
16.6
通讯作者：
Gong Z
中科院分区：
文献类型：
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作者：
Kong L;Cheng J;Zhu Y;Ding Y;Meng J;Chen Z;Xie Q;Guo Y;Li J;Yang S;Gong Z
支链A蛋白磷酸酶2Cs(PP2Cs)是脱落酸(ABA)的辅受体，通过抑制下游的蛋白激酶来阻断ABA信号转导。在拟南芥中，PP2Cs被ABA结合的PYR/PYL/RCAR ABA受体(PYR/PYL/RCAR ABA受体)抑制后ABA信号被激活。然而，这些PP2C是否受到其他因素的调节仍是未知的。在这里，我们报道ABI1(ABA不敏感的1)可以与U-box E3连接酶PUB12和PUB13相互作用，但只有在体外实验中它与ABA受体相互作用时才被泛素化。不能与幽门螺杆菌相互作用的ABI1-1突变形式比野生型蛋白更稳定。与野生型相比，pub12 pub13突变体的ABI1降解和所有测试的ABA反应都减少了。将abi1-3功能缺失突变引入pub12pub13突变体，恢复了pub12pub13突变体的ABA不敏感表型。因此，我们揭示了PUB12和PUB13调节ABI1水平的重要调控机制。植物激素脱落酸(ABA)的信号转导受ABI1蛋白磷酸酶的调节。在这里，孔令辉等人。提出ABI1泛素化可以微调ABA信号，促进ABI对ABA的降解。
Clade A protein phosphatase 2Cs (PP2Cs) are abscisic acid (ABA) co-receptors that block ABA signalling by inhibiting the downstream protein kinases. ABA signalling is activated after PP2Cs are inhibited by ABA-bound PYR/PYL/RCAR ABA receptors (PYLs) in Arabidopsis. However, whether these PP2Cs are regulated by other factors remains unknown. Here, we report that ABI1 (ABA-INSENSITIVE 1) can interact with the U-box E3 ligases PUB12 and PUB13, but is ubiquitinated only when it interacts with ABA receptors in an in vitro assay. A mutant form of ABI1-1 that is unable to interact with PYLs is more stable than the wild-type protein. Both ABI1 degradation and all tested ABA responses are reduced in pub12 pub13 mutants compared with the wild type. Introducing the abi1-3 loss-of-function mutation into pub12 pub13 mutant recovers the ABA-insensitive phenotypes of the pub12 pub13 mutant. We thus uncover an important regulatory mechanism for regulating ABI1 levels by PUB12 and PUB13. Signaling by the plant hormone abscisic acid (ABA) is regulated by the ABI1 protein phosphatase. Here Kong et al. propose that ABA signaling is fine-tuned by ubiquitination of ABI1 which promotes ABI degradation in response to ABA.