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TGA 结合因子 1(TGA1)和 TGA4 通过调节系统性获得性抗性缺陷 1(SARD1)和钙调素结合蛋白 60g(CBP60g)的表达来调节水杨酸和吡咯啉酸的生物合成。

TGACG-BINDING FACTOR 1 (TGA1) and TGA4 regulate salicylic acid and pipecolic acid biosynthesis by modulating the expression of SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60g (CBP60g).

机构信息

Department of Botany, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada.

Department of Chemistry, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada.

出版信息

New Phytol. 2018 Jan;217(1):344-354. doi: 10.1111/nph.14780. Epub 2017 Sep 12.

Abstract

Salicylic acid (SA) and pipecolic acid (Pip) play important roles in plant immunity. Here we analyzed the roles of transcription factors TGACG-BINDING FACTOR 1 (TGA1) and TGA4 in regulating SA and Pip biosynthesis in Arabidopsis thaliana. We quantified the expression levels of SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60g (CBP60g), which encode two master transcription factors of plant immunity, and the accumulation of SA and Pip in tga1-1 tga4-1 mutant plants. We tested whether SARD1 and CBP60g are direct targets of TGA1 by chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR). In addition to promoting pathogen-induced SA biosynthesis, we found that SARD1 and CBP60g also positively regulated Pip biosynthesis by targeting genes encoding key biosynthesis enzymes of Pip. TGA1/TGA4 were required for full induction of SARD1 and CBP60g in plant defense. ChIP-PCR analysis showed that SARD1 was a direct target of TGA1. In tga1-1 tga4-1 mutant plants, the expression levels of SARD1 and CBP60g along with SA and Pip accumulation following pathogen infection were dramatically reduced compared with those in wild-type plants. Consistent with reduced expression of SARD1 and CBP60g, pathogen-associated molecular pattern (PAMP)-induced pathogen resistance and systemic acquired resistance were compromised in tga1-1 tga4-1. Our study showed that TGA1 and TGA4 regulate Pip and SA biosynthesis by modulating the expression of SARD1 and CBP60g.

摘要

水杨酸(SA)和吡咯啉-5-羧酸(Pip)在植物免疫中发挥重要作用。在这里,我们分析了转录因子 TGACG-结合因子 1(TGA1)和 TGA4 在调节拟南芥 SA 和 Pip 生物合成中的作用。我们定量分析了系统性获得性抗性缺陷 1(SARD1)和钙调蛋白结合蛋白 60g(CBP60g)的表达水平,这两种蛋白编码植物免疫的两个主要转录因子,以及 tga1-1 tga4-1 突变体植物中 SA 和 Pip 的积累情况。我们通过染色质免疫沉淀聚合酶链反应(ChIP-PCR)测试了 SARD1 和 CBP60g 是否是 TGA1 的直接靶标。除了促进病原体诱导的 SA 生物合成外,我们还发现 SARD1 和 CBP60g 通过靶向编码 Pip 生物合成关键酶的基因,也正向调节 Pip 生物合成。TGA1/TGA4 是植物防御中 SARD1 和 CBP60g 完全诱导所必需的。ChIP-PCR 分析表明 SARD1 是 TGA1 的直接靶标。在 tga1-1 tga4-1 突变体植物中,与野生型植物相比,病原体感染后 SARD1 和 CBP60g 的表达水平以及 SA 和 Pip 的积累量均显著降低。与 SARD1 和 CBP60g 的表达减少一致,tga1-1 tga4-1 中病原体相关分子模式(PAMP)诱导的病原体抗性和系统获得性抗性受到损害。我们的研究表明,TGA1 和 TGA4 通过调节 SARD1 和 CBP60g 的表达来调节 Pip 和 SA 的生物合成。

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