The Marssonina rosae effector MrSEP43 suppresses immunity in rose by targeting the orphan protein RcBROG
Journal of Experimental Botany, ISSN: 1460-2431, Vol: 75, Issue: 16, Page: 4993-5007
2024
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Most Recent News
Researchers from Beijing Forestry University Report New Studies and Findings in the Area of Botany (The Marssonina Rosae Effector Mrsep43 Suppresses Immunity In Rose By Targeting the Orphan Protein Rcbrog)
2024 JUL 02 (NewsRx) -- By a News Reporter-Staff News Editor at NewsRx Life Science Daily -- Current study results on Life Sciences - Botany
Article Description
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 responses by secreting effectors. However, the molecular mechanism involved in inhibition of the rose immune response by M. rosae effectors remains poorly understood. Here, we identified the effector MrSEP43, which plays a pivotal role in promoting the virulence of M. rosae and enhancing rose susceptibility to infection by reducing callose deposition, HO accumulation, and the expression of defense genes in the jasmonic acid signaling pathway. Yeast two-hybrid, bimolecular fluorescence complementation, and split luciferase assays showed that MrSEP43 interacted with the rose orphan protein RcBROG. RcBROG, a positive regulator of defense against M. rosae, enhanced rose resistance by increasing callose deposition, HO accumulation, and the expression of RcERF1 in the ethylene signaling pathway. Overall, our findings suggest that the M. rosae virulence effector MrSEP43 specifically targets the orphan protein RcBROG to suppress the rose immune response to M. rosae. These results provide new insights into how M. rosae manipulates and successfully colonizes rose leaves, and are essential for preventing the breakdown of resistance to rose black spot disease.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85202650299&origin=inward; http://dx.doi.org/10.1093/jxb/erae200; http://www.ncbi.nlm.nih.gov/pubmed/38706346; https://academic.oup.com/jxb/article/75/16/4993/7665233; https://dx.doi.org/10.1093/jxb/erae200; https://academic.oup.com/jxb/advance-article/doi/10.1093/jxb/erae200/7665233
Oxford University Press (OUP)
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