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Cotton GhSSI2 isoforms from the stearoyl acyl carrier protein fatty acid desaturase family regulate Verticillium wilt resistance
Molecular Plant Pathology ( IF 4.9 ) Pub Date : 2021-06-24 , DOI: 10.1111/mpp.13093
Shaojing Mo 1 , Yan Zhang 1 , Xingfen Wang 1 , Jun Yang 1 , Zhengwen Sun 1 , Dongmei Zhang 1 , Bin Chen 1 , Guoning Wang 1 , Huifeng Ke 1 , Zhengwen Liu 1 , Chengsheng Meng 1 , Zhikun Li 1 , Liqiang Wu 1 , Guiyin Zhang 1 , Huijun Duan 1 , Zhiying Ma 1
Affiliation  

Lipids are major and essential constituents of plant cells and provide energy for various metabolic processes. However, the function of the lipid signal in defence against Verticillium dahliae, a hemibiotrophic pathogen, remains unknown. Here, we characterized 19 conserved stearoyl-ACP desaturase family proteins from upland cotton (Gossypium hirsutum). We further confirmed that GhSSI2 isoforms, including GhSSI2-A, GhSSI2-B, and GhSSI2-C located on chromosomes A10, D10, and A12, respectively, played a dominant role to the cotton 18:1 (oleic acid) pool. Suppressing the expression of GhSSI2s reduced the 18:1 level, which autoactivated the hypersensitive response (HR) and enhanced cotton Verticillium wilt and Fusarium wilt resistance. We found that low 18:1 levels induced phenylalanine ammonia-lyase-mediated salicylic acid (SA) accumulation and activated a SA-independent defence response in GhSSI2s-silenced cotton, whereas suppressing expression of GhSSI2s affected PDF1.2-dependent jasmonic acid (JA) perception but not the biosynthesis and signalling cascade of JA. Further investigation showed that structurally divergent resistance-related genes and nitric oxide (NO) signal were activated in GhSSI2s-silenced cotton. Taken together, these results indicate that SA-independent defence response, multiple resistance-related proteins, and elevated NO level play an important role in GhSSI2s-regulated Verticillium wilt resistance. These findings broaden our knowledge regarding the lipid signal in disease resistance and provide novel insights into the molecular mechanism of cotton fungal disease resistance.

中文翻译:

来自硬脂酰基载体蛋白脂肪酸去饱和酶家族的棉花 GhSSI2 异构体调节黄萎病抗性

脂质是植物细胞的主要和必需成分,为各种代谢过程提供能量。然而,脂质信号在防御黄萎病菌(一种半营养性病原体)中的功能仍然未知。在这里,我们从陆地棉 ( Gossypium hirsutum ) 中表征了 19 种保守的硬脂酰-ACP 去饱和酶家族蛋白。我们进一步证实了GhSSI2亚型,包括分别位于染色体 A10、D10 和 A12 上的 GhSSI2-AGhSSI2-BGhSSI2-C,对棉花 18:1(油酸)池起主导作用。抑制GhSSI2的表达s 降低 18:1 水平,自动激活过敏反应 (HR) 并增强棉花黄萎病和枯萎病的抗性。我们发现低 18:1 水平诱导苯丙氨酸解氨酶介导的水杨酸 (SA) 积累并激活GhSSI2 s 沉默棉花中的 SA 非依赖性防御反应,而抑制GhSSI2 s 的表达影响 PDF1.2 依赖性茉莉酸(JA) 感知,但不是 JA 的生物合成和信号级联。进一步的研究表明,结构上不同的抗性相关基因和一氧化氮 (NO) 信号在GhSSI2 s中被激活-消音棉。总之,这些结果表明不依赖 SA 的防御反应、多种抗性相关蛋白和升高的 NO 水平在GhSSI2 s调节黄萎病抗性中起重要作用。这些发现拓宽了我们对抗病脂质信号的认识,并为棉花抗真菌病的分子机制提供了新的见解。
更新日期:2021-08-12
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