VfLRR-RLK1 benefiting resistance to Fusarium oxysporum reveals infection and defense mechanisms in tung tree.

Abstract

Fusarium wilt, caused by Fusarium oxysporum f. sp. fordiis in Vernicia fordii, manifests as severe symptoms that significantly reduce global tung oil yield. However, the molecular-mechanisms of the Vernicia-Fusarium interaction are yet to be fully elucidated. Here, we cloned VfLRR-RLK1 from tung tree roots, which contained 1134 bp, encoding 378 AA. To further analyze VfLRR-RLK1 function in resistance to Fusarium wilt, we obtained stable T4-generation transgenic Arabidopsis thaliana and tung tree VfLRR-RLK1 virus-induced gene silencing (VIGS) RNAi plants. A. thaliana plants overexpressing VfLRR-RLK1 exhibited more robust root development and markedly increased Fusarium wilt disease resistance. In response to Fusarium wilt stress, transgenic A. thaliana exhibited increased catalase (CAT) and superoxide dismutase (SOD) enzyme activities, while showing reduced O₂ ^- and hydrogen peroxide (H₂O₂) accumulation. The findings suggest that VfLRR-RLK1 may diminish plant reactive oxygen species (ROS) levels and foster root development by activating the ROS antioxidant scavenging system during plant Pattern Triggered Immunity responses, enhancing resistance to Fusarium wilt. The study on the function of VfLRR-RLK1 is crucial in breeding programs aimed at developing tung tree resistant to Fusarium wilt, and lays the groundwork for more effective disease management strategies and the cultivation of tung tree varieties with enhanced resistance to this disease.

Supplementary information: The online version contains supplementary material available at 10.1007/s12298-024-01512-y.