SlATG5 is crucial for the accumulation of ROS in postharvest tomato fruit resistance to B.cinerea mediated by nitric oxide

Abstract

Autophagy is a highly conserved intracellular degradation process that effectively eliminates damaged cells caused by various stresses, including pathogens. While nitric oxide (NO) as the initial signaling molecule in enhancing disease resistance is known, the potential molecular mechanism between autophagy and NO remains elusive. In this study, knockout of SlATG5 intensified the symptoms of disease and promoted the accumulation of reactive oxygen species (ROS). In addition, NO increased the expression of SlATG5, and the absence of SlATG5 also reduced the content of NO and the activity of NOS enzyme. More importantly, knockout of SlATG5 reduced the positive role of NO in disease resistance, which is accompanied with lower enzyme activity of CHI and PPO, and higher level of ROS in SNP+slatg5 compared to SNP+WT. In addition, SlATG5 induced the response of ethylene and auxin signaling. After the deletion of SlATG5, the expressions of ethylene receptors ETR3 and ETR5 were significantly up-regulated, and the auxin-related genes SlIAA1, SlIAA12, and SlIAA17 were significantly inhibited. Thus, our data demonstrate that SlATG5 participates in NO-induced tomato fruit resistance against B.cinerea and induces the response of ethylene and auxin signaling.