Cotton GhMKK5-GhMPK13 cascade regulates resistance to Verticillium wilt by phosphorylating GhBES1- GhPEL75- mediated molecular module

Abstract

Verticillium wilt caused by Verticillium dahliae is a soil-borne vascular disease that harms many plants, including cotton. Mitogen-activated protein kinase (MAPK) cascade is a highly conserved signal transduction pathway that transmits various extracellular stimuli to downstream targets during plant defense responses. Though there have been many studies on the key role of MAPK cascade in plant disease resistance, the MAPK signal transduction in cotton remains to be elucidated. Here, we found that GhMKK5 interacted with GhMPK13 and directly phosphorylated GhMPK13. Silencing the homologs GbMKK5 or GbMPK13 in Gossypium barbadense acc. Hai7124 significantly compromised resistance to V. dahliae, accompanied by reduced MAPK phosphorylation levels. Conversely, overexpression of GhMKK5 in Arabidopsis enhanced disease resistance and increased phosphorylation of AtMPK3/6. GhMPK13 can phosphorylate BRI1-EMS-SUPPRESSOR 1 (GhBES1), a core transcription factor in the brassinosteroid signaling pathway, which plays a negative regulator in resistance to V. dahliae by regulating the expression of pectate lyase 75 (GhPEL75). The phosphorylation of GhBES1 diminishes the binding ability to the promoter of GhPEL75, leading to the reduction of pectate lyase activity and enhanced disease resistance in cotton. In addition, another interacting protein of GhMPK13, GhSRC1 could improve the stability of GhMPK13 and silencing of its expression decreased the resistance to V. dahliae. Taken together, our results propose a MAPK pathway of GhMKK5-GhMPK13-GhBES1-GhPEL75 in the regulation of resistance to Verticillium wilt in cotton, providing insights into the molecular mechanisms underlying plant cell wall adaptive alteration in the defense response.