The Marssonina rosae effector MrSEP43 suppresses rose immunity by targeting the orphan protein RcBROG.
Yi YangYucen QiLin SuShumin YangXingwan YiLe LuoChao YuTangren ChengJia WangQixiang ZhangHuitang PanPublished in: Journal of experimental botany (2024)
Rose black spot disease, caused by Marssonina rosae (syn. Diplocarpon rosae), is one of the most widespread diseases of field-grown roses worldwide. Pathogens have been found to interfere with or stimulate plant immune response through the secreted effectors. However, the molecular mechanism involved in inhibition of rose immune response by M. rosae effectors remains poorly understood. In this study, we identified the effector MrSEP43, which played a pivotal role in promoting the virulence of M. rosae and enhancing rose susceptibility by reducing callose deposition, H2O2 accumulation, and the expression of defense genes in jasmonic acid signaling pathway. Through Y2H, BiFC, and LUC assays, MrSEP43 was proved to interact with the rose orphan protein RcBROG. RcBROG, which was a positive regulator of defense against M. rosae, enhanced rose resistance by increasing callose deposition, H2O2 accumulation, and expression of RcERF1 in the ethylene signaling pathway. Overall, our findings suggested that the virulence effector MrSEP43 from M. rosae specifically targeted the orphan protein RcBROG to suppress rose immune response to M. rosae. These results provided new insight into how M. rosae manipulated and successfully colonized rose leaves, and were essential for preventing the breakdown of resistance to rose black spot disease.
Keyphrases
- signaling pathway
- immune response
- dendritic cells
- binding protein
- escherichia coli
- poor prognosis
- type iii
- pseudomonas aeruginosa
- regulatory t cells
- staphylococcus aureus
- pi k akt
- antimicrobial resistance
- epithelial mesenchymal transition
- gene expression
- biofilm formation
- drug delivery
- small molecule
- induced apoptosis
- oxidative stress
- inflammatory response
- toll like receptor
- cancer therapy
- endoplasmic reticulum stress
- genome wide identification