Location: Sugarbeet and Potato ResearchTitle: Identification and characterization of Cercospora beticola necrosis-inducing effector CbNip1
|EBERT, MALAIKA - North Dakota State University|
|DE JONGE, RONNIE - Utrecht University|
|SECOR, GARY - North Dakota State University|
|THOMMA, BART - University Of Cologne|
Submitted to: Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/9/2020
Publication Date: 2/5/2021
Citation: Ebert, M.K., Rangel, L., Wang, X., Friesen, T.L., De Jonge, R., Neubauer, J., Secor, G., Thomma, B., Bolton, M.D. 2021. Identification and characterization of Cercospora beticola necrosis-inducing effector CbNip1. Molecular Plant Pathology. 22:301-316. https://doi.org/10.1111/mpp.13026.
Interpretive Summary: The fungus Cercospora beticola causes a serious disease of sugar beet worldwide called Cercospora leaf spot. In this research, we identify and describe a new protein that causes cell death in sugar beet plants. This protein relies on periods of darkness to fully cause cell death. When the gene encoding this protein is removed from the Cercospora beticola genome, the fungus is severely impacted in its ability to grow on sugarbeet, causing very little disease. The identification of a new pathogen protein that is critical for cell death and disease in sugar beet will be useful for plant breeders to select varieties based on resistance to the protein identified in this study. This knowledge will also be useful for plant pathologists to understand how organisms like Cercospora cause disease in other crop plants.
Technical Abstract: Cercospora beticola is a hemibiotrophic fungus that causes Cercospora leaf spot disease of sugar beet (Beta vulgaris L.). After an initial symptom-free biotrophic phase of colonization, necrotic lesions appear on host leaves as the fungus switches to a necrotrophic lifestyle. The phytotoxic secondary metabolite cercosporin has been shown to facilitate fungal virulence for several Cercospora spp. However, since cercosporin production and subsequent cercosporin-initiated formation of reactive oxygen species is light-dependent, cell death evocation by this toxin is only fully ensured during a period of light. Here, we report the discovery of the effector protein CbNip1 secreted by C. beticola that causes enhanced necrosis in the absence of light and therefore may complement light-depended necrosis formation by cercosporin. Infiltration of CbNIP1 protein into sugar beet leaves revealed that darkness is essential for full CbNIP1-triggered necrosis, as light exposure delayed CbNIP1-triggered host cell death. Gene expression analysis during host infection shows that CbNip1 expression is correlated with symptom development in planta. Targeted gene replacement of CbNip1 leads to a significant reduction in virulence indicating the importance of CbNIP1 during colonization. Pull-down analysis with heterologously produced CbNIP1 identified several candidate interaction partners.