GhNAC043 and GhBPM2 interaction enhances Verticillium wilt resistance in cotton through jasmonic acid and abscisic acid pathways.
TL;DR
A previously unknown regulatory pathway in which the GhNAC043-GhBPM2 complex drives lignin deposition through the modulation of JA and ABA signaling, thereby fortifying cotton against VW infection is highlighted.
Abstract
The soil-borne fungal pathogen Verticillium dahliae (V. dahliae) is the causal agent of Verticillium wilt (VW), a vascular disease that severely threatens global cotton production. Although cell wall lignification represents a cornerstone of plant immunity, the precise regulatory circuits that bridge this structural reinforcement with Verticillium dahliae resistance in cotton have yet to be fully elucidated. Here, we demonstrate that the NAC transcription factor GhNAC043 is a key positive regulator of this defense. GhNAC043 expression was rapidly induced upon V. dahliae infection. Silencing GhNAC043 in cotton compromised resistance, reducing lignin accumulation and downregulating lignin biosynthesis genes. Conversely, heterologous overexpression of GhNAC043 in Arabidopsis enhanced VW tolerance. We further identified GhBPM2 as a nuclear interaction partner of GhNAC043. Profiling of the transcriptome demonstrated that the GhNAC043-GhBPM2 module alters the expression profile of genes pivotal for jasmonic acid (JA) and abscisic acid (ABA) signal transduction. Collectively, these results highlight a previously unknown regulatory pathway in which the GhNAC043-GhBPM2 complex drives lignin deposition through the modulation of JA and ABA signaling, thereby fortifying cotton against VW infection.