枯萎病
尖孢镰刀菌
生物
几丁质酶
基因沉默
植物抗病性
转录因子
基因表达
基因
微生物学
遗传学
分子生物学
作者
Ezra S. Bartholomew,Shuo Xu,Yaqi Zhang,Shuai Yin,Zhongxuan Feng,Shuyinq Chen,Lei Sun,Songlin Yang,Ying Wang,Peng Liu,Huazhong Ren,Xingwang Liu
摘要
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.
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