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<p>Rose black leaf lesion is one of the most severe diseases affecting roses compromising both the growth and ornamental value of rose plants. In this study, <i>Marssonina rosae</i> and <i>Alternaria alternata</i> were persistently isolated from rose leaves exhibiting black leaf lesion disease symptoms, with their pathogenicity confirmed using Koch's postulates. In dual culture assays, <i>M. rosae</i> and <i>A. alternata</i> were co-cultured for their preliminary characterization, and the liquid culture filtrate of <i>M. rosae</i> stimulated the growth of <i>A. alternata</i>. To investigate fungal interactions, detached leaves were first inoculated with <i>M. rosae</i>, then with <i>A. alternata</i> at 0-, 4-, or 6-day intervals, whereas control groups received single inoculations. Results demonstrated that pre-inoculation of <i>M. rosae</i> four days prior to <i>A. alternata</i> significantly increased both lesion area and <i>M. rosae</i> spore density on leaves. Comparative gene expression analyses were performed of several genes involved in the plant’s reactions to the pathogens, such as the master regulators of salicylic acid (SA) or jasmonic acid (JA)-mediated defense signaling pathway networks. In susceptible roses, elevated SA levels during early <i>M. rosae</i> infection (0-4 dpi) suppressed SA-related defense signaling, concurrently inhibiting pathogen interaction genes (<i>OPR3, ICS, NPR1, MYC2, WRKY70</i>) and facilitating <i>A. alternata</i> invasion. During later stages (8-10 dpi), declining SA-related gene expression attenuated SA-JA antagonism, enhancing <i>M. rosae</i> pathogenicity/sporulation. This study reveals that the co-infection by two fungi aggravates disease severity via SA-JA pathway manipulation to promote the invasion of <i>A. alternaria</i> and further enhance the pathogenicity of <i>M. rosae</i>. The findings elucidate a novel mechanism underlying rose black leaf lesion epidemiology, establishing a theoretical foundation for improved disease management.</p>

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Co-infection by Marssonina rosae and Alternaria alternata alters host responses of rose black leaf lesion disease

  • 期刊论文

  • 发表日期：

    2025年7月3日

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  • Chaowei Liang,
  • Hongying Shan,
  • Huiqin Liu,
  • Hongchun Liang,
  • Zhaorong Chen

摘要

Rose black leaf lesion is one of the most severe diseases affecting roses compromising both the growth and ornamental value of rose plants. In this study, Marssonina rosae and Alternaria alternata were persistently isolated from rose leaves exhibiting black leaf lesion disease symptoms, with their pathogenicity confirmed using Koch's postulates. In dual culture assays, M. rosae and A. alternata were co-cultured for their preliminary characterization, and the liquid culture filtrate of M. rosae stimulated the growth of A. alternata. To investigate fungal interactions, detached leaves were first inoculated with M. rosae, then with A. alternata at 0-, 4-, or 6-day intervals, whereas control groups received single inoculations. Results demonstrated that pre-inoculation of M. rosae four days prior to A. alternata significantly increased both lesion area and M. rosae spore density on leaves. Comparative gene expression analyses were performed of several genes involved in the plant’s reactions to the pathogens, such as the master regulators of salicylic acid (SA) or jasmonic acid (JA)-mediated defense signaling pathway networks. In susceptible roses, elevated SA levels during early M. rosae infection (0-4 dpi) suppressed SA-related defense signaling, concurrently inhibiting pathogen interaction genes (OPR3, ICS, NPR1, MYC2, WRKY70) and facilitating A. alternata invasion. During later stages (8-10 dpi), declining SA-related gene expression attenuated SA-JA antagonism, enhancing M. rosae pathogenicity/sporulation. This study reveals that the co-infection by two fungi aggravates disease severity via SA-JA pathway manipulation to promote the invasion of A. alternaria and further enhance the pathogenicity of M. rosae. The findings elucidate a novel mechanism underlying rose black leaf lesion epidemiology, establishing a theoretical foundation for improved disease management.