大丽花黄萎病
黄萎病
茉莉酸
生物
生物合成
脱落酸
植物抗病性
司他内酯
信号转导
转录组
生物化学
细胞生物学
植物
酶
突变体
基因
拟南芥
基因表达
作者
Yifei Han,Yue Sun,Sheng Wang,Huazu Li,Meng Jiang,Xueying Liu,Yuefen Cao,Wanru Wang,Hong Yin,Jinhong Chen,Jie Sun,Qian‐Hao Zhu,Shuijin Zhu,Tianlun Zhao
摘要
ABSTRACT Verticillium wilt (VW) caused by the soil‐borne fungal pathogen Verticillium dahliae reduces cotton productivity and quality. Numerous studies have explored the genetic and molecular mechanisms regulating VW resistance in cotton, but the role and mechanism of strigolactone (SL) is still elusive. We investigated the function of SL in cotton's immune response to V. dahliae infection by exogenously applying SL analog, blocking or enhancing biosynthesis of endogenous SLs in combination with comparative transcriptome analysis and by exploring cross‐talk between SL and other phytohormones. Silencing GhDWARF27 and applying the SL analog GR24 or overexpressing GhDWARF27 decreased and enhanced V. dahliae resistance, respectively. Transcriptome analysis revealed SL‐mediated activation of abscisic acid (ABA) and jasmonic acid (JA) biosynthesis and signaling pathways. Enhanced ABA biosynthesis and signaling led to increased activity of antioxidant enzymes and reduced buildup of excess reactive oxygen species. Enhanced JA biosynthesis and signaling facilitated transcription of JA–dependent disease resistance genes. One of the components of the SL signal transduction pathway, GhD53, was found to interact with GhNCED5 and GhLOX2, the key enzymes of ABA and JA biosynthesis, respectively. We revealed the molecular mechanism underlying SL–enabled V. dahliae resistance and provided potential solutions for improving VW resistance in cotton.
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