학술논문

Biosynthesis and Signaling of Strigolactones Act Synergistically With That of ABA and JA to Enhance Verticillium dahliae Resistance in Cotton (Gossypium hirsutum L.).
Document Type
Article
Source
Plant, Cell & Environment. Jan2025, Vol. 48 Issue 1, p571-586. 16p.
Subject
Language
ISSN
0140-7791
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. Summary statement: VW caused by Verticillium dahliae reduces cotton productivity and quality. Our study demonstrated that SLs are positive regulators of V. dahliae resistance, established the cross‐talk relationship between SLs and JA/ABA and provided insight into the molecular mechanism underlying SL–mediated disease resistance. [ABSTRACT FROM AUTHOR]