Arabidopsis transcription factor WRKY8 functions antagonistically with its interacting partner VQ9 to modulate salinity stress tolerance
Arabidopsis transcription factor WRKY8 functions antagonistically with its interacting partner VQ9 to modulate salinity stress tolerance
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DOI：
10.1111/tpj.12159
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发表时间：
2013-06-01
期刊：
影响因子：
7.2
通讯作者：
Yu, Diqiu
中科院分区：
文献类型：
--
作者：
Hu, Yanru;Chen, Ligang;Yu, Diqiu
WRKY转录因子已被证明在调节应激反应中起着至关重要的作用;然而，它们参与应激反应的确切机制尚未完全了解。拟南芥WRKY 8主要在根中表达，并且通过盐处理高度上调。WRKY 8的破坏使植物对盐过敏，表现出延迟发芽，抑制发芽后的发展和加速褪绿。进一步的研究表明，WRKY 8与VQ 9相互作用，它们的相互作用降低了WRKY 8的DNA结合活性。VQ 9蛋白仅定位于细胞核中，并且VQ 9表达强烈响应于NaCl处理。VQ 9的突变增强了对盐胁迫的耐受性，表明VQ 9与WRKY 8拮抗作用以介导对盐胁迫的响应。WRKY 8和VQ 9的拮抗剂功能与增加或减少的Na+/K+浓度比以及盐胁迫wrky 8和vq 9突变体中下游胁迫响应基因的表达模式的对比一致。此外，染色质免疫沉淀（ChIP）分析表明，WRKY 8直接结合的RD 29 A在盐条件下的启动子。这些结果提供了强有力的证据表明，VQ 9蛋白作为WRKY 8因子的阻遏物，以维持WRKY 8介导的信号传导途径的适当平衡，从而建立盐胁迫耐受性。
The WRKY transcription factors have been demonstrated to play crucial roles in regulating stress responses; however, the exact mechanisms underlying their involvement in stress responses are not fully understood. Arabidopsis WRKY8 was predominantly expressed in roots and was highly upregulated by salt treatment. Disruption of WRKY8 rendered plants hypersensitive to salt, showing delayed germination, inhibited post-germination development and accelerated chlorosis. Further investigation revealed that WRKY8 interacted with VQ9, and their interaction decreased the DNA-binding activity of WRKY8. The VQ9 protein was exclusively localized in the nucleus, and VQ9 expression was strongly responsive to NaCl treatment. Mutation of VQ9 enhanced tolerance to salt stress, indicating that VQ9 acts antagonistically with WRKY8 to mediate responses to salt stress. The antagonist functions of WRKY8 and VQ9 were consistent with an increased or reduced Na+/K+ concentration ratio, as well as contrasting expression patterns of downstream stress-responsive genes in salt-stressed wrky8 and vq9 mutants. Moreover, chromatin immunoprecipitation (ChIP) assays showed that WRKY8 directly bound the promoter of RD29A under salt conditions. These results provided strong evidence that the VQ9 protein acts as a repressor of the WRKY8 factor to maintain an appropriate balance of WRKY8-mediated signaling pathways to establish salinity stress tolerance.