Salt responsive alternative splicing of a RING finger E3 ligase modulates the salt stress tolerance by fine-tuning the balance of COP9 signalosome subunit 5A.
Salt responsive alternative splicing of a RING finger E3 ligase modulates the salt stress tolerance by fine-tuning the balance of COP9 signalosome subunit 5A.
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RING Finger E3 连接酶的盐响应选择性剪接通过微调 COP9 信号体亚基 5A 的平衡来调节盐胁迫耐受性
DOI：
10.1371/journal.pgen.1009898
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发表时间：
2021-11
期刊：
影响因子：
4.5
通讯作者：
Yan K
中科院分区：
文献类型：
--
作者：
Zhou Y;Li XH;Guo QH;Liu P;Li Y;Wu CA;Yang GD;Huang JG;Zhang SZ;Zheng CC;Yan K
越来越多的证据表明，选择性剪接（AS）与植物的盐胁迫反应密切相关。然而，将这两种现象联系起来的机制仍不清楚。在这项研究中，我们发现，盐响应替代剪接基因1（SRAS 1），编码一个环型E3连接酶，产生两个剪接变体：SRAS1.1和SRAS1.2，表现出相反的反应，盐胁迫。盐胁迫响应的AS事件导致SRAS1.1的更大积累和SRAS1.2的更低水平。综合表型分析表明，SRAS1.1的过表达使植物对盐胁迫更耐受，而SRAS1.2的过表达使它们更敏感。此外，我们成功地鉴定了COP 9信号体5A（CSN 5A）作为SRAS 1的靶标。CSN 5A在植物发育和胁迫调节中起着重要作用。全长SRAS1.1促进26 S蛋白酶体对CSN 5A的降解。相比之下，SRAS1.2通过与SRAS1.1竞争相同的结合位点来保护CSN 5A。因此，盐胁迫触发的AS控制SRAS1.1/SRAS1.2的比例，并开启和关闭CSN 5A的降解，以平衡植物的发育和耐盐性。总之，这些结果提供的见解，盐响应AS作为转录后调节介导的E3连接酶的功能。
Increasing evidence points to the tight relationship between alternative splicing (AS) and the salt stress response in plants. However, the mechanisms linking these two phenomena remain unclear. In this study, we have found that Salt-Responsive Alternatively Spliced gene 1 (SRAS1), encoding a RING-Type E3 ligase, generates two splicing variants: SRAS1.1 and SRAS1.2, which exhibit opposing responses to salt stress. The salt stress-responsive AS event resulted in greater accumulation of SRAS1.1 and a lower level of SRAS1.2. Comprehensive phenotype analysis showed that overexpression of SRAS1.1 made the plants more tolerant to salt stress, whereas overexpression of SRAS1.2 made them more sensitive. In addition, we successfully identified the COP9 signalosome 5A (CSN5A) as the target of SRAS1. CSN5A is an essential player in the regulation of plant development and stress. The full-length SRAS1.1 promoted degradation of CSN5A by the 26S proteasome. By contrast, SRAS1.2 protected CSN5A by competing with SRAS1.1 on the same binding site. Thus, the salt stress-triggered AS controls the ratio of SRAS1.1/SRAS1.2 and switches on and off the degradation of CSN5A to balance the plant development and salt tolerance. Together, these results provide insights that salt-responsive AS acts as post-transcriptional regulation in mediating the function of E3 ligase.
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