ArticleBMC plant biology2022
Identification of effector CEP112 that promotes the infection of necrotrophic Alternaria solani.
Article in BMC plant biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Alternaria alternata Effector Aa593 Promotes Virulence by Hijacking the CmNAC29-Mediated Abscisic Acid Biosynthesis Pathway in Chrysanthemum.Plant biotechnology journal · 2026Article
- Mechanisms of action and biocontrol potential ofFrontiers in fungal biology · 2026Review
- Reactive oxygen species production and signal transduction in response to stress triggered by Alternaria elicitors in Brassicaceae.Plant molecular biology · 2025Review
- A glycosylphosphatidylinositol-anchored protein from Alternaria alternata triggers cell death and negatively modulates immunity responses in chrysanthemum.Plant cell reports · 2024Article
- Network analyses predict major regulators of resistance to early blight disease complex in tomato.BMC plant biology · 2024Article
- Alternaria diseases on potato and tomato.Molecular plant pathology · 2024Review
- Transcriptome sequencing leads to an improved understanding of the infection mechanism of Alternaria solani in potato.BMC plant biology · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlternaria solani is a typical necrotrophic pathogen that can cause severe early blight on Solanaceae crops and cause ring disease on plant leaves. Phytopathogens produce secretory effectors that regulate the host immune response and promote pathogenic infection. Effector proteins, as specialized secretions of host-infecting pathogens, play important roles in disrupting host defense systems. At present, the role of the effector secreted by A. solani during infection remains unclear. We report the identification and characterization of AsCEP112, an effector required for A. solani virulence.
resultThe AsCEP112 gene was screened from the transcriptome and genome of A. solani on the basis of typical effector signatures. Fluorescence quantification and transient expression analysis showed that the expression level of AsCEP112 continued to increase during infection. The protein localized to the cell membrane of Nicotiana benthamiana and regulated senescence-related genes, resulting in the chlorosis of N. benthamiana and tomato leaves. Moreover, comparative analysis of AsCEP112 mutant obtained by homologous recombination with wild-type and revertant strains indicated that AsCEP112 gene played an active role in regulating melanin formation and penetration in the pathogen. Deletion of AsCEP112 also reduced the pathogenicity of HWC-168.
conclusionOur findings demonstrate that AsCEP112 was an important effector protein that targeted host cell membranes. AsCEP112 regulateed host senescence-related genes to control host leaf senescence and chlorosis, and contribute to pathogen virulence.
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