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一个几丁质酶 CsChi23 启动子多态性是黄瓜抗黄瓜枯萎病菌的基础。

A chitinase CsChi23 promoter polymorphism underlies cucumber resistance against Fusarium oxysporum f. sp. cucumerinum.

机构信息

College of Horticulture, China Agricultural University, Beijing, 100193, China.

Heze Agricultural and Rural Bureau, No. 1021 Shuanghe Road, Mudan District, Heze City, Shandong, 274000, China.

出版信息

New Phytol. 2022 Nov;236(4):1471-1486. doi: 10.1111/nph.18463. Epub 2022 Sep 30.

DOI:10.1111/nph.18463
PMID:36068958
Abstract

Fusarium wilt disease, caused by Fusarium oxysporum f. sp. cucumerinum (Foc), leads to widespread yield loss and quality decline in cucumber. However, the molecular mechanisms underlying Foc resistance remain poorly understood. We report the mapping and functional characterisation of CsChi23, encoding a cucumber class I chitinase with antifungal properties. We assessed sequence variations at CsChi23 and the associated defence response against Foc. We functionally characterised CsChi23 using transgenic assay and expression analysis. The mechanism regulating CsChi23 expression was assessed by genetic and molecular approaches. CsChi23 was induced by Foc infection, which led to rapid upregulation in resistant cucumber lines. Overexpressing CsChi23 enhanced fusarium wilt resistance and reduced fungal biomass accumulation, whereas silencing CsChi23 causes loss of resistance. CsHB15, a homeodomain leucine zipper (HD-Zip) III transcription factor, was found to bind to the CsChi23 promoter region and activate its expression. Furthermore, silencing of CsHB15 reduces CsChi23 expression. A single-nucleotide polymorphism variation -400 bp upstream of CsChi23 abolished the HD-Zip III binding site in a susceptible cucumber line. Collectively, our study indicates that CsChi23 is sufficient to enhance fusarium wilt resistance and reveals a novel function of an HD-Zip III transcription factor in regulating chitinase expression in cucumber defence against fusarium wilt.

摘要

镰刀菌枯萎病由尖孢镰刀菌黄瓜专化型(Foc)引起,导致黄瓜广泛减产和品质下降。然而,Foc 抗性的分子机制仍知之甚少。我们报告了编码具有抗真菌特性的黄瓜 I 类几丁质酶的 CsChi23 的定位和功能特征。我们评估了 CsChi23 序列变异及其与防御 Foc 的关联。我们通过转基因试验和表达分析对 CsChi23 进行了功能表征。通过遗传和分子方法评估了调节 CsChi23 表达的机制。Foc 感染诱导 CsChi23 的表达,导致抗性黄瓜品系中迅速上调。过表达 CsChi23 增强了枯萎病抗性并减少了真菌生物量的积累,而沉默 CsChi23 则导致抗性丧失。CsHB15 是一个同源域亮氨酸拉链(HD-Zip)III 转录因子,被发现与 CsChi23 启动子区域结合并激活其表达。此外,CsHB15 的沉默降低了 CsChi23 的表达。在易感黄瓜品系中,CsChi23 上游 -400bp 的单核苷酸多态性变异消除了 HD-Zip III 结合位点。总之,我们的研究表明 CsChi23 足以增强枯萎病抗性,并揭示了 HD-Zip III 转录因子在调节黄瓜防御枯萎病中几丁质酶表达的新功能。

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