Abstract: Tomato (Solanum lycopersicum) is an important crop but frequently experiences saline–alkali stress. Our previous studies have shown that exogenous spermidine (Spd) could significantly enhance the saline–alkali resistance of tomato seedlings, in which a high concentration of Spd and jasmonic acid (JA) exerted important roles. However, the mechanism of Spd and JA accumulation remains unclear. Herein, SlWRKY42, a Group II WRKY transcription factor, was identified in response to saline–alkali stress. Overexpression of SlWRKY42 improved tomato saline–alkali tolerance. Meanwhile, SlWRKY42 knockout mutants, exhibited an opposite phenotype. RNA-sequencing data also indicated that SlWRKY42 regulated the expression of genes involved in JA signaling and Spd synthesis under saline–alkali stress. SlWRKY42 is directly bound to the promoters of SlSPDS2 and SlNHX4 to promote Spd accumulation and ionic balance, respectively. SlWRKY42 interacted with SlMYC2. Importantly, SlMYC2 is also bound to the promoter of SlSPDS2 to promote Spd accumulation and positively regulated saline–alkali tolerance. Furthermore, the interaction of SlMYC2 with SlWRKY42 boosted SlWRKY42's transcriptional activity on SlSPDS2, ultimately enhancing the tomato's saline–alkali tolerance. Overall, our findings indicated that SlWRKY42 and SlMYC2 promoted saline–alkali tolerance by the Spd biosynthesis pathway. Thus, this provides new insight into the mechanisms of plant saline–alkali tolerance responses triggered by polyamines (PAs).

Key words: jasmonic acid, saline‐alkali stress, SlMYC2, SlWRKY42, spermidine, tomato