ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Phytophthora Disrupts Plant Immunity by Manipulating Nitric Oxide Homeostasis Through GSNOR Inhibition.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Hydrogen Gas Enhances Salinity Tolerance in Tomato Seedlings by Regulating the S-Nitrosylation of MEK1.Plant biotechnology journal · 2026Article
- The Central Role of GSNOR: Decoding Nitric Oxide Signaling for Crop Stress Tolerance.International journal of molecular sciences · 2025Review
- Phytophthora Disrupts Plant Immunity by Manipulating Nitric Oxide Homeostasis Through GSNOR Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Nitric oxide (NO), a pivotal redox signaling molecule, coordinates plant development and immune responses through S-nitrosylation-mediated protein modification. While NO-dependent S-nitrosylation fine-tunes immune responses, whether pathogens hijack this process to subvert plant immunity remains unclear. Here it is shown that S-nitrosoglutathione reductase (GSNOR), which maintains NO homeostasis by degrading S-nitrosoglutathione (GSNO), positively regulates tomato resistance to Phytophthora capsici. Active-site mutations in GSNOR abolished its function in plant defense. Remarkably, GSNOR is manipulated by PcRD18, which is an RxLR effector of P. capsici that is involved in virulence of this oomycete pathogen. PcRD18 elevates the cellular NO content and S-nitrosylation levels by dually inhibiting GSNOR activity and promoting its autophagy-mediated degradation via enhanced ATG8c interaction. Structure analysis reveals critical PcRD18-GSNOR interaction interfaces and mutations in these sites of PcRD18 abolish its ability to interact with GSNOR, thereby blocking the effector's ability to elevate NO levels, suppress the reactive oxygen species (ROS) burst, and enhance virulence. GSNOR mutations disrupting PcRD18 binding produced a mutant form of GSNOR enhancing Phytophthora resistance. These findings unveil a pathogen strategy to subvert NO homeostasis through effector-mediated hijacking of GSNOR and suggest that engineering the host-pathogen interface to disrupt the interaction between GSNOR and PcRD18 will enhance crop disease resistance.
Indexed as
Identifiers
What OpenQuestion holds
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.