ArticlePLoS pathogens2020
Verticillium dahliae chromatin remodeling facilitates the DNA damage repair in response to plant ROS stress.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 65 citations in OpenAlex.
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- Microorganisms' perception, scavenging, and adaptation to reactive oxygen species signals in microbe-plant interactions.World journal of microbiology & biotechnology · 2025Review
- Mitochondrial Complex Member VdNuo1 Recruits Superoxide Dismutases VdSOD2/4 to Maintain Superoxide Anion Homeostasis During Pathogenesis in Verticillium dahliae.Molecular plant pathology · 2025Article
- PsDMAP1/PsTIP60-regulated H4K16ac is required for ROS-dependent virulence adaptation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic landscape underlying plant-microbiome chemical communication.The ISME journal · 2025Review
- Structural and functional characterisation and regulatory mechanisms of SWI/SNF and RSC chromatin remodelling complexes in fungi.Mycology · 2025Review
- Enhanced oxidative stress resistance in Ustilago maydis and its implications on the virulence.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- Transcription factors containing both CmSphere · 2024Article
- Root-knot nematodes exploit the catalase-like effector to manipulate plant reactive oxygen species levels by directly degrading HMolecular plant pathology · 2024Article
- The novel roles of RNA m6A modification in regulating the development, infection, and oxidative DNA damage repair of Phytophthora sojae.PLoS pathogens · 2024Article
- The dynamics and functional mechanisms of H2B mono-ubiquitination.Crop health · 2024Review
- VirulentFrontiers in plant science · 2024Article
- A combined transcriptomic and physiological approach to understanding the adaptive mechanisms to cope with oxidative stress inMicrobiology spectrum · 2023Article
- DeSUMOylation of a Verticillium dahliae enolase facilitates virulence by derepressing the expression of the effector VdSCP8.Nature communications · 2023Article
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- Thioredoxin VdTrx1, an unconventional secreted protein, is a virulence factor inFrontiers in microbiology · 2023Article
- A DEK domain-containing protein GhDEK2D mediatedPlant signaling & behavior · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) production is one of the earliest responses when plants percept pathogens and acts as antimicrobials to block pathogen entry. However, whether and how pathogens tolerate ROS stress remains elusive. Here, we report the chromatin remodeling in Verticillium dahliae, a soil-borne pathogenic fungus that causes vascular wilts of a wide range of plants, facilitates the DNA damage repair in response to plant ROS stress. We identified VdDpb4, encoding a histone-fold protein of the ISW2 chromatin remodeling complex in V. dahliae, is a virulence gene. The reduced virulence in wild type Arabidopsis plants arising from VdDpb4 deletion was impaired in the rbohd mutant plants that did not produce ROS. Further characterization of VdDpb4 and its interacting protein, VdIsw2, an ATP-dependent chromatin-remodeling factor, we show that while the depletion of VdIsw2 led to the decondensing of chromatin, the depletion of VdDpb4 resulted in a more compact chromatin structure and affected the VdIsw2-dependent transcriptional effect on gene expression, including genes involved in DNA damage repair. A knockout mutant of either VdDpb4 or VdIsw2 reduced the efficiency of DNA repair in the presence of DNA-damaging agents and virulence during plant infection. Together, our data demonstrate that VdDpb4 and VdIsw2 play roles in maintaining chromatin structure for positioning nucleosomes and transcription regulation, including genes involved in DNA repair in response to ROS stress during development and plant infection.
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