Botrytis cinerea uses effective detoxification mechanisms to overcome the plant RBOHD-dependent extracellular oxidative burst
4 affiliations
- 1Plant Pathology, Department of Biology, University of Kaiserslautern-Landau
- 2Institute of Plant Sciences, Plant RNA Biotechnology, University of Regensburg
- 3Molecular Botany, Department of Biology, University of Kaiserslautern-Landau
- 4Genomics & Transcriptomics Labor (BMFZ), Heinrich-Heine-University
Abstract
The necrotrophic fungus Botrytis cinerea rapidly kills host tissue with its secreted proteins and metabolites. Necrotrophs can trigger the hypersensitive response, which is accompanied by reactive oxygen species (ROS) production, but it remains unclear whether this ROS burst promotes or restricts B. cinerea infection. We have combined Arabidopsis RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) mutant analysis, luminol-based in vivo assays, and the use of CRISPR/Cas9-generated B. cinerea ROS detoxification mutants to analyze the toxic effect of the ROS burst. In addition, RNA-sequencing, transcript analyses and redox imaging were used to study RBOHD-dependent signaling and redox homeostasis. RBOHD mutants showed slightly increased susceptibility to B. cinerea infection, and the apoplastic ROS burst was found to be dependent on RBOHD. Fungal mutants confirmed the importance of SOD1 and AP1 for ROS detoxification and virulence. Unexpectedly, the transcriptomes of B. cinerea -infected Arabidopsis Col-0 and an activation-impaired RBOHD mutant were highly similar 48 hours after inoculation, providing no evidence for a connection of extracellular ROS production and intracellular ROS-induced transcriptional signaling. Nevertheless, RBOHD activity was found to be involved in the maintenance of cellular redox homeostasis under phytotoxic stress. Our results indicate a protective role of the RBOHD-dependent oxidative burst against B. cinerea , but this can be overcome by the fungus via different ROS detoxification mechanisms.
Related
- MSC-derived extracellular vesicles for spinal cord injury: inflammatory microenvironment modulation, stage-dependent repair mechanisms, and translational challenges
- Ligand-Dependent Associations of the Bovine TLR2 R152Q Variant with Neutrophil Oxidative Burst, Extracellular DNA Release, and Innate Immune Gene Expression
- Multiomic Profiling Links RDH12-Dependent Retinaldehyde Detoxification to Membrane Remodeling and Ferroptosis
- Oxidative Stress in Lactuca sativa L.: Cellular Mechanisms, Stress Responses, and Mitigation Strategies
- Neutrophil Extracellular Traps at the Asthma + COPD Interface: Mechanisms, Experimental Models, and Therapeutic Targeting
BibTeX
@article{vielbafernandez2026botrytis,
title = {{Botrytis cinerea uses effective detoxification mechanisms to overcome the plant RBOHD-dependent extracellular oxidative burst}},
author = {Alejandra Vielba-Fernandez and Lea Sommer and Désirée Ross and Julian Ingelfinger and Thorsten Wachtmeister and Jochen Hecht and Nassim Safari and Stefanie J Müller-Schüssele and Matthias Hahn},
journal = {Frontiers in Plant Science},
year = {2026},
month = oct,
doi = {10.3389/fpls.2026.1969467},
url = {https://www.frontiersin.org/articles/10.3389/fpls.2026.1969467/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Botrytis cinerea uses effective detoxification mechanisms to overcome the plant RBOHD-dependent extracellular oxidative burst
AU - Alejandra Vielba-Fernandez
AU - Lea Sommer
AU - Désirée Ross
AU - Julian Ingelfinger
AU - Thorsten Wachtmeister
AU - Jochen Hecht
AU - Nassim Safari
AU - Stefanie J Müller-Schüssele
AU - Matthias Hahn
PY - 2026
DA - 2026/10/16
JO - Frontiers in Plant Science
DO - 10.3389/fpls.2026.1969467
UR - https://www.frontiersin.org/articles/10.3389/fpls.2026.1969467/full
AB - The necrotrophic fungus Botrytis cinerea rapidly kills host tissue with its secreted proteins and metabolites. Necrotrophs can trigger the hypersensitive response, which is accompanied by reactive oxygen species (ROS) production, but it remains unclear whether this ROS burst promotes or restricts B. cinerea infection. We have combined Arabidopsis RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) mutant analysis, luminol-based in vivo assays, and the use of CRISPR/Cas9-generated B. cinerea ROS detoxification mutants to analyze the toxic effect of the ROS burst. In addition, RNA-sequencing, transcript analyses and redox imaging were used to study RBOHD-dependent signaling and redox homeostasis. RBOHD mutants showed slightly increased susceptibility to B. cinerea infection, and the apoplastic ROS burst was found to be dependent on RBOHD. Fungal mutants confirmed the importance of SOD1 and AP1 for ROS detoxification and virulence. Unexpectedly, the transcriptomes of B. cinerea -infected Arabidopsis Col-0 and an activation-impaired RBOHD mutant were highly similar 48 hours after inoculation, providing no evidence for a connection of extracellular ROS production and intracellular ROS-induced transcriptional signaling. Nevertheless, RBOHD activity was found to be involved in the maintenance of cellular redox homeostasis under phytotoxic stress. Our results indicate a protective role of the RBOHD-dependent oxidative burst against B. cinerea , but this can be overcome by the fungus via different ROS detoxification mechanisms.
SN - 1664-462X
ER -