GhCOR27 Confers Verticillium Wilt Resistance in Cotton by Relieving the GhASIL1- GhERF114 -Mediated Repression of Lignin Accumulation

Verticillium wilt (VW) severely limits cotton production, yet the molecular mechanisms underlying cotton immunity remain incompletely understood. Here, comparative transcriptomic analyses of resistant and susceptible cotton germplasms identified the cold-regulated gene GhCOR27 as a positive regulator of VW resistance. GhCOR27 expression was consistently induced by Verticillium dahliae infection in both resistant and susceptible materials. Functional validation showed that silencing GhCOR27 enhanced susceptibility, whereas its overexpression in cotton and Arabidopsis markedly improved VW resistance. Through yeast two-hybrid (Y2H), bimolecular fluorescence complementation (BiFC), luciferase complementation (LCI), co-immunoprecipitation (Co-IP) and GST pull-down, we further demonstrated that GhCOR27 directly interacts with the trihelix transcription factor GhASIL1. Silencing and overexpression in Arabidopsis revealed GhASIL1 acts as a negative regulator of VW resistance. Transcriptome profiling indicated that GhCOR27 and GhASIL1 coregulate the phenylpropanoid pathway, lignin accumulation, and ROS/NO signaling during defense. Mechanistically, DNA affinity purification sequencing (DAP-seq), yeast one-hybrid (Y1H), dual-luciferase (LUC) and electrophoretic mobility shift assay (EMSA) assays revealed that GhASIL1 directly binds the GT-box cis-element in the promoter of GhERF114, a defense-related transcription factor, and represses its expression. Importantly, GhCOR27 antagonizes GhASIL1-mediated repression of GhERF114 without binding to the GhERF114 promoter itself. Subsequently, GhERF114 activates the expression of the lignin biosynthetic gene GhHCT1, thereby promoting lignification and strengthening disease resistance. Together, we conclude that GhCOR27 confers VW resistance in cotton by relieving the GhASIL1-GhERF114-mediated repression of lignin accumulation, which provide a new insight into the molecular mechanisms of cotton defense against VW.