E2 conjugases UBC1 and UBC2 regulate MYB42-mediated SOS pathway in response to salt stress in Arabidopsis
E2 conjugases UBC1 and UBC2 regulate MYB42-mediated SOS pathway in response to salt stress in Arabidopsis
复制标题
E2 结合物 UBC1 和 UBC2 调节 MYB42 介导的 SOS 通路以响应拟南芥盐胁迫
DOI：
10.1111/nph.16538
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发表时间：
2020-04-19
期刊：
影响因子：
9.4
通讯作者：
Li, Yingzhang
中科院分区：
文献类型：
--
作者：
Sun, Yuhui;Zhao, Jun;Li, Yingzhang
组蛋白H_2B单素化(H_2Bub1)被认为是真核生物中一种重要的调控机制，在发育和适应环境变化的过程中控制着一系列的细胞过程。在拟南芥中，E2结合酶泛素载体蛋白(UBCs)-1和-2介导了H_2B的泛素化。在此，我们阐明了Ubc1和-2在盐胁迫反应中的功能，并揭示了它们的下游靶基因。实时定量PCR分析表明，Ubc1和-2正向调节盐诱导的MYB42和丝裂原激活蛋白激酶4(MPK4)的表达。染色质免疫沉淀分析表明，突变株中H_2Bub1在MYB42和MPK4染色质上有微弱的富集性。我们进一步确定了在盐胁迫条件下，Ubc1/2介导的H2Bub1增加了MYB42和MPK4染色质中K4(H3K4me3)上三甲基化的组蛋白H3的水平。MPK4介导的MYB42磷酸化增强了MYB42蛋白在盐胁迫条件下的稳定性和转录活性。我们进一步证明了MYB42直接与盐过度敏感2(SOS2)启动子结合，并在盐处理后介导其表达的快速诱导。我们的结果表明，UBC1和-2通过调节MYB42介导的SOS2的表达来积极地调节盐胁迫反应。
Histone H2B monoubiquitination (H2Bub1) is recognized as a crucial eukaryotic regulatory mechanism that controls a range of cellular processes during both development and adaptation to environmental changes. In Arabidopsis, the E2 conjugated enzymes UBIQUITIN CARRIER PROTEINs (UBCs) -1 and -2 mediate ubiquitination of H2B. Here, we elucidated the functions of UBC1 and -2 in salt-stress responses and revealed their downstream target genes.Real-time quantitative PCR assays showed that UBC1 and -2 positively regulated the salt-induced expression of MYB42 and Mitogen-Activated Protein Kinase 4 (MPK4). Chromatin immunoprecipitation assays revealed that H2Bub1 was enriched weakly on the chromatin of MYB42 and MPK4 in the ubc1,2 mutant. We further determined that UBC1/2-mediated H2Bub1 enhanced the level of histone H3 tri-methylated on K4 (H3K4me3) in the chromatin of MYB42 and MPK4 under salt-stress conditions.MPK4 interacted with and phosphorylated MYB42. The MPK4-mediated MYB42 phosphorylation enhanced the MYB42 protein stability and transcriptional activity under salt-stress conditions. We further showed that MYB42 directly bound to the SALT OVERLY SENSITIVE 2 (SOS2) promoter and mediated the rapid induction of its expression after a salt treatment.Our results indicate that UBC1 and -2 positively regulate salt-stress responses by modulating MYB42-mediated SOS2 expression.