Genome-wide identification and characterization of WRKYs family involved in responses to Cylindrocarpon destructans in Panax notoginseng.

BACKGROUND

WRKY transcription factors (TFs) are key regulators of plant responses to biotic and abiotic stresses. Previous studies demonstrated that the role of WRKY TFs play in the disease resistance of Panax notoginseng, the causal agent of root rot disease. However, comprehensive genome-wide analyses of WRKY genes in this species remain scarce.

RESULT

We identified 79 WRKY genes in the P. notoginseng genome, classifing them into three groups based on structural features and phylogenetic relationships: Class I (14 genes), Class II (55 genes), and Class III (10 genes). Of these, 58 PnWRKY genes were mapped to the P. notoginseng chromosomes and showed collinearity with Arabidopsis thaliana, Daucus carota, and three Solanaceae species. Expression analysis revealed that 53 PnWRKY genes were actively transcribed across various tissues, including roots, flowers, stems, rhizomes, and different root parts. Furthermore, PnWRKY genes responded to Cylindrocarpon destructans infection and were induced by jasmonic acid (JA) and salicylic acid (SA). Notably, the ectopic expression of PnWRKY35 in tobacco enhanced resistance to C. destructans, accompanied by increased levels of gibberellins (GA, GA, GA), JA, SA, and brassinolide. KEGG enrichment analysis of 547 differentially expressed genes (DEGs) indicated their involvement pathways related to disease resistance, including the biosynthesis of sesquiterpenes and triterpenes, JA biosynthesis, plant-pathogen interactions and the MAPK signaling pathway.

CONCLUSION

This study demonstrated that the WRKY family in P. notoginseng plays a significant role in resistance to root rot disease. PnWRKY genes are responsive to MeJA and SA induction as well as C. destructans infection. Moreover, ectopic expression of PnWRKY35 activates multiple plant disease resistance pathways, increases phytohormone levels, and enhance resistance to C. destructans. These findings provide a foundation for future exploration of the mechanism underlying P. notoginseng resistance to root rot disease.