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Plant J：擬南芥WRKY8與VQ9調節鹽脅迫耐受性
2006~2020，NMT已扎根中國15年。2020年，中國NMT銷往瑞士蘇黎世大學，正式打開歐洲市場。
NMT歷*的今天
2013年03月02日，中科院西雙版納熱帶植物園余迪求、胡彥如用NMT在Plant Journal上發表了標題為Arabidopsis transcription factor WRKY8 functions antagonistically with its interacting partner VQ9 to modulate salinity stress tolerance的研究成果。
期刊：Plant Journal
主題：擬南芥WRKY8與VQ9調節鹽脅迫耐受性
標題：Arabidopsis transcription factor WRKY8 functions antagonistically with its interacting partner VQ9 to modulate salinity stress tolerance
影響因子：6.582
檢測指標：K+流速
作者：中科院西雙版納熱帶植物園余迪求、胡彥如
英文摘要
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.
中文摘要（谷歌機翻）
WRKY轉錄因子已被證明在調節壓力反應中起關鍵作用。然而，它們參與應激反應的確切機制尚不*清楚。
擬南芥WRKY8主要在根中表達，并通過鹽處理高度上調。WRKY8的破壞使植物對鹽高度敏感，表現出延遲的發芽，抑制了發芽后的發育并加速了萎黃病。進一步的研究表明，WRKY8與VQ9相互作用，并且它們的相互作用降低了WRKY8的DNA結合活性。
VQ9蛋白專門位于細胞核中，并且VQ9表達對NaCl處理有強烈反應。VQ9突變增強了對鹽脅迫的耐受性，表明VQ9與WRKY8拮抗，介導對鹽脅迫的響應。WRKY8和VQ9的拮抗劑功能與Na+ / K+濃度比的增加或降低，以及鹽脅迫的wrky8和vq9突變體中下游脅迫反應基因的相反表達模式一致。
此外，染色質免疫沉淀（ChIP）分析表明，WRKY8在鹽條件下直接結合RD29A的啟動子。這些結果提供了有力的證據，表明VQ9蛋白可作為WRKY8因子的阻遏物，以維持WRKY8介導的信號通路的適當平衡，從而建立鹽度脅迫耐受性。
(c) Net K+ ef?ux in root tips. Seeds were germinated on MS agar medium for 4 days in a vertical manner. The net immediate K+ ef?ux was measured using the non-injuring technique after the addition of salt. The insert shows the mean ef?ux rates within the measuring period of 0–20 min.