SlNPR1 modulates chilling stress resistance in tomato plant by alleviating oxidative damage and affecting the synthesis of ferulic acid

Abstract

• NPR1 gene and protein content are dramatically induced by chilling stress. • CRISPR/Cas9-mediated SlNPR1 inhibition aggravated the symptoms of chilling injury. • SlNPR1 enhances tolerance to chilling stress by alleviating oxidative damage. • SlNPR1 enhances tolerance to chilling stress by affecting the synthesis of FA. Non-expresser of pathogenesis-related genes 1 (NPR1) has been demonstrated to be a master transcription factor during resistance against pathogens, the mechanisms by which regulates chilling stress, however, remain unclear. Our results revealed that the expression and protein content of SlNPR1 were dramatically induced by low temperature (4 °C). CRISPR/Cas9-mediated SlNPR1 mutagenesis aggravated the symptoms of chilling injury in tomato plant, which was accompanied with the accumulation of malonic dialdehyde (MDA), hydrogen peroxide (H 2 O 2 ) and superoxide anion (O 2 − ), and the decrease of soluble protein content, proline content as well as antioxidant enzymes activity. In addition, slnpr1 mutants showed lower expression of SlICE1 and SlCBF1 in contrast to wild type plants (WT) . PAL, C4H, C3H and COMT genes play important roles in the synthesis of ferulic acid (FA). We found that knockout of SlNPR1 reduced the expression of PAL, C4H, C3H and COMT induced by low temperature (4 °C) and inhibited the accumulation of FA content. Interestingly, FA-treated plants showed greater tolerance to chilling stress and displayed higher expression of SlICE1 and SlCBF1 , exhibited lower levels of MDA and H 2 O 2 , but higher antioxidant enzyme (APX, POD, SOD and CAT) activity than WT. These findings reveal a new regulatory pathway that SlNPR1 enhances tolerance to chilling stress in tomato plant by alleviating oxidative damage and affecting the synthesis of FA.