ArticlePlant signaling & behavior2010
ROS signaling in the hypersensitive response: when, where and what for?
Article in Plant signaling & behavior, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
85 citing papers in PubMed, 177 citations in OpenAlex.
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- A New Approach for CRISPR/Cas9 Editing and Selection of Pathogen-Resistant Plant Cells of Wine Grape cv. 'Merlot'.International journal of molecular sciences · 2024Article
- Roles of Reactive Carbonyl Species (RCS) in Plant Response to Abiotic Stress.Methods in molecular biology (Clifton, N.J.) · 2024Article
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- The same boat, different storm: stress volatile emissions in response to biotrophic fungal infections in primary and alternate hosts.Plant signaling & behavior · 2023Article
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25 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plants generally react to the attack of non-host and incompatible host microorganisms by inducing pathogenesis-related (PR) genes and localised cell death (LCD) at the site of infection, a process collectively known as the hypersensitive response (HR). Reactive oxygen species (ROS) are generated in various sub-cellular compartments shortly after pathogen recognition, and proposed to cue subsequent orchestration of the HR. Although apoplast-associated ROS production by plasma membrane NADPH oxidases have been most thoroughly studied, recent observations suggest that ROS are generated in chloroplasts earlier in the response and play a key role in execution of LCD. A model is presented in which the initial outcome of successful pathogen detection is ROS accumulation in plastids, likely mediated by mitogen-activated protein kinases and caused by dysfunction of the photosynthetic electron transport chain. ROS signaling is proposed to spread from plastids to the apoplast, through the activation of NADPH oxidases, and from there to adjacent cells, leading to suicidal death in the region of attempted infection.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.