MdWRKY15 improves resistance of apple to Botryosphaeria dothidea via the salicylic acid‐mediated pathway by directly binding the MdICS1 promoter
Isochorismate synthase (ICS) plays an essential role in the accumulation of salicylic acid (SA) and plant disease resistance. Diseases caused by Botryosphaeria dothidea affect apple yields. Thus, it is important to understand the role of ICS1 in disease resistance to B. dothidea in apple. In this st...
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Veröffentlicht in: | Journal of integrative plant biology 2020-04, Vol.62 (4), p.527-543 |
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Zusammenfassung: | Isochorismate synthase (ICS) plays an essential role in the accumulation of salicylic acid (SA) and plant disease resistance. Diseases caused by Botryosphaeria dothidea affect apple yields. Thus, it is important to understand the role of ICS1 in disease resistance to B. dothidea in apple. In this study, SA treatment enhanced the resistance to B. dothidea. MdICS1 was induced by B. dothidea and enhanced the resistance to B. dothidea. MdICS1 promoter analysis indicated that the W‐box was vital for the response to B. dothidea treatment. MdWRKY15 was found to interact with the W‐box using yeast one‐hybrid screening. Subsequently, the interaction was confirmed by EMSA, yeast one‐hybrid, ChIP‐PCR, and quantitative PCR assays. Moreover, luciferase and GUS analysis further indicated that MdICS1 was transcriptionally activated by MdWRKY15. Finally, we found the function of MdWRKY15 in the resistance to B. dothidea was partially dependent on MdICS1 from the phenotype of transgenic apples and calli. In summary, we revealed that MdWRKY15 activated the transcription of MdICS1 by directly binding to its promoter to increase the accumulation of SA and the expression of disease‐related genes, thereby resulting in the enhanced resistance to B. dothidea in the SA biosynthesis pathway.
Diseases caused by Botryosphaeria dothidea affect apple yields. Here we report that MdWRKY15 and MdICS1 could enhance the resistance of apple to Botryosphaeria dothidea by increasing the accumulation of SA and the expression of disease‐related genes in a SA‐mediated manner. |
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ISSN: | 1672-9072 1744-7909 |
DOI: | 10.1111/jipb.12825 |