Recently, a research team led by Professor Li Fuguang from the Cotton Research Institute of the Chinese Academy of Agricultural Sciences revealed the molecular mechanism by which the effector Vd6317 from Verticillium dahliae suppresses plant defenses against verticillium wilt. This provides important molecular evidence for the breeding and improvement of disease-resistant cotton. The research findings were published in the international authoritative academic journal "The Plant Journal" (IF=6.2, Biology Q1) under the title "Suppression of plant immunity by Verticillium dahliae effector Vd6317 through AtNAC53 association."

Verticillium dahliae, a soil-borne fungal pathogen, compromises host innate immunity by secreting a plethora of effectors, thereby facilitating host colonization and causing substantial yield and quality losses. The mechanisms underlying the modulation of cotton immunity by  V. dahliae  effectors are predominantly unexplored. In this study, we identified that the  V. dahliae  effector Vd6317 inhibits plant cell death triggered by Vd424Y and enhances PVX viral infection in  Nicotiana benthamiana . Attenuation of Vd6317 significantly decreased the virulence of  V. dahliae , whereas ectopic expression of Vd6317 in Arabidopsis and cotton enhanced susceptibility to  V. dahliae  infection, underscoring Vd6317's critical role in pathogenicity. We observed that Vd6317 targeted the Arabidopsis immune regulator AtNAC53, thereby impeding its transcriptional activity on the defense-associated gene  AtUGT74E2 . Arabidopsis  nac53  and  ugt74e2  mutants exhibited heightened sensitivity to  V. dahliae  compared to wild-type plants. A mutation at the conserved residue 193L of Vd6317 abrogated its interaction with AtNAC53 and reduced the virulence of  V. dahliae , which was partially attributable to a reduction in Vd6317 protein stability. Our findings unveil a hitherto unrecognized regulatory mechanism by which the  V. dahliae  effector Vd6317 directly inhibits the plant transcription factor AtNAC53 activity to suppress the expression of  AtUGT74E2  and plant defense.

This work was financially supported by National Key R&D Program of China (2022YFF1001400), National Natural Science Foundation of China (32201731), Innovation Program of Chinese Academy of Agricultural Sciences (CAAS-CSIAF-202402).

https://doi.org/10.1111/tpj.16883