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LysM effectors are suppressors of chitin-triggered plant immunity in biotrophic and hemibiotrophic fungi. In necrotrophic fungi, LysM effectors might induce a mechanism to suppress host immunity during the short asymptomatic phase they establish before these fungi activate plant defenses and induce host cell death leading to necrosis. Here, we characterize a secreted LysM protein from a major necrotrophic fungus, Botrytis cinerea, called BcLysM1. Transcriptional induction of BcLysM1 gene was observed in multicellular appressoria, called infection cushions, in unicellular appressoria and in the early phase of infection on bean leaves. We confirmed that BcLysM1 protein binds chitin in the fungus cell wall and protects hyphae against degradation by external chitinases. This effector is also able to suppress the chitin-induced ROS burst in Arabidopsis thaliana, suggesting sequestration of chitooligosaccharides in apoplast during infection. Moreover, contribution of BcLysM1 in infection initiation and in adhesion to bean leaf surfaces were demonstrated. Our data show for the first time that a LysM effector can play a dual role in mycelial adhesion and suppression of chitin-triggered host immunity, both of which occur during the early asymptomatic phase of infection by necrotrophic fungi.
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http://dx.doi.org/10.1002/jobm.202400552 | DOI Listing |
Allergy
August 2025
College of Veterinary Medicine, Biosafety Research Institute and Core Facility Center for Zoonosis Research, Jeonbuk National University, Iksan, Republic of Korea.
Background: Asthma exacerbations caused by human rhinovirus (hRV) infection are characterized by airway neutrophilia and reduced corticosteroid response, leading to significant healthcare costs and lung function impairment. The Gαs subunit of the trimeric G protein regulates immunopathological conditions by modulating cAMP levels. We aimed to investigate the impact of myeloid cAMP levels on neutrophil-dominated asthma exacerbation caused by hRV infection.
View Article and Find Full Text PDFbioRxiv
May 2025
Wellcome Discovery Research Platforms in Infections, Centre for Infectious Diseases Research in Africa (CIDRI-Africa), Institute of Infectious Diseases and Molecular Medicine (IDM), Faculty of Health Sciences, University of Cape Town, Cape Town 7925, Republic of South Africa.
A host-modulating candidate gene involved in putative pathogen-killing pathways, with potential novel therapeutic intervention, Protein Kinase C - δ (PKCδ) has been recognized as a critical marker of inflammation with clinical and experimental evidence in recent years. Pulmonary microenvironment during infection is largely governed by lung resident macrophages, initiating innate and subsequent adaptive immune responses. We investigated the role of PKCδ in macrophages using a macrophage-specific PKCδ knockout mice model (LysMPKCδ).
View Article and Find Full Text PDFNat Microbiol
June 2025
Department of Molecular Microbiology, Center for Women's Infectious Disease Research, Washington University School of Medicine, St Louis, MO, USA.
Inflammation is critical for controlling infections but can cause disease when unchecked. During Mycobacterium tuberculosis (Mtb) infection, neutrophil-dominated inflammation is associated with exacerbated disease. ATG5 expression by neutrophils mediates autophagy-independent control of infection but mechanistic understanding of how this regulates protective neutrophil function is lacking.
View Article and Find Full Text PDFSci Rep
April 2025
Department of Medicine, Section of Pulmonary and Critical Care Medicine, The University of Chicago, 5841 S. Maryland Avenue MC6026, Chicago, IL, 60637, USA.
HIF-1α plays a critical role in shaping macrophage phenotype and effector function. We have previously shown that tissue-resident alveolar macrophages (TR-AMs) have extremely low glycolytic capacity at steady-state but can shift toward glycolysis under hypoxic conditions. Here, we generated mice with tamoxifen-inducible myeloid lineage cell specific deletion of Hif1a (Hif1a:LysM-CreERT2) and from these mice, we isolated TR-AMs and bone marrow-derived macrophages (BMDMs) in which Hif1a is deleted.
View Article and Find Full Text PDFFront Plant Sci
January 2025
Indian River Research and Education Center, Department of Plant Pathology, Institute of Food and Agricultural Sciences (IFAS), University of Florida, Fort Pierce, FL, United States.
, the causal agent of anthracnose fruit rot, is globally recognized as a major pathogen of strawberries due to its economic impact. Fungal pathogens utilize secreted proteins to facilitate infection by acquiring host nutrients and suppressing plant immunity. Understanding the transcriptomic responses of during infection can provide critical insights into its pathogenic mechanisms.
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