Salinity is a universal environmental stress that causes yield reduction in plants. WRKY33, which has been extensively studied in plant defense against necrotrophic pathogens, has recently been found to be important in salt-responsive pathways. However, the underlying molecular mechanisms controlling the involvement of WRKY33 in salt tolerance have not been fully characterized. Here, we explored the function of BcWRKY33A in non-heading Chinese Cabbage (NHCC). Under salt stress, BcWRKY33A expression is significantly induced in roots. As a nuclear protein, BcWRKY33A has strong transcriptional activation activity. Overexpression of BcWRKY33A confers salt tolerance in Arabidopsis, whereas silencing of BcWRKY33A causes salt sensitivity in NHCC. Furthermore, BcHSFA4A, a protein that interacts with BcWRKY33A, could directly bind to the HSE motif within the promoters of BcZAT12 and BcHSP17.6A, which are involved in the plant response to salt stress. Finally, we found that BcWRKY33A could enhance the transcriptional activity of BcHSFA4A and affect its downstream genes (e.g. BcZAT12 and BcHSP17.6A), and co-overexpression of BcWRKY33A and BcHSFA4A could promote the expression of salt-related genes, suggesting that the regulatory interaction between BcWRKY33A and BcHSFA4A improves salt tolerance in plants. Overall, our results provide insight into the molecular framework of the BcWRKY33A-BcHSFA4A signaling pathway, which also aids in our understanding of the salt tolerance molecular mechanism in plants.
The transcription factor WRKY33 is a vital regulator of the biological process of the necrotrophic fungus Botrytis cinerea (B. cinerea). However, its specific regulatory mechanism remains to be further investigated. In non-heading Chinese cabbage (NHCC, Brassica campestris (syn. Brassica rapa) ssp. Chinensis), our previous study showed that BcWRKY33A is induced not only by salt stress, but also by B. cinerea infection. Here, we noticed that BcWRKY33A is expressed in trichomes and confer plant defense resistance. Disease symptoms and qRT-PCR analyses revealed that BcWRKY33A-overexpressing and -silencing lines were less and more severely impaired, respectively, than wild type upon B. cinerea treatment. Meanwhile, the transcripts’ abundance of indolic glucosinolates’ (IGSs) biosynthetic genes is consistent with plants’ B. cinerea tolerance. Identification and expression pattern analysis of BcMYB51s showed that BcMYB51-3 has a similar trend to BcWRKY33A upon B. cinerea infection. Moreover, BcWRKY33A directly binds to the BcMYB51-3 promoter, which was jointly confirmed by Y1H, dual-LUC, and EMSA assays. The importance of MYB51, the homolog of BcMYB51-3, in the BcWRKY33A-mediated B. cinerea resistance was also verified using the TRV-based VIGS system. Overall, our data concludes that BcWRKY33A directly activates the expression of BcMYB51-3 and downstream IGSs’ biosynthetic genes, thereby improving the B. cinerea tolerance of NHCC plants.
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