ArticlePLoS genetics2017
The GYF domain protein PSIG1 dampens the induction of cell death during plant-pathogen interactions.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Biomolecular condensates as cellular memory modules: Thermodynamic principles and plant stress adaptation.Biophysical journal · 2026Review
- Genome-wide identification and expression profiling of theFrontiers in plant science · 2026Article
- MaSMG7-Mediated Degradation of MaERF12 FacilitatesInternational journal of molecular sciences · 2024Article
- A translational regulator MHZ9 modulates ethylene signaling in rice.Nature communications · 2023Article
- Interaction of EXA1 and eIF4E Family Members Facilitates Potexvirus Infection in Arabidopsis thaliana.Journal of virology · 2023Article
- The genomic and epigenetic footprint of local adaptation to variable climates in kiwifruit.Horticulture research · 2023Article
- Article
- Plantago asiatica mosaic virus: An emerging plant virus causing necrosis in lilies and a new model RNA virus for molecular research.Molecular plant pathology · 2022Review
- Creativity comes from interactions: modules of protein interactions in plants.The FEBS journal · 2022Review
- Susceptibility factor StEXA1 interacts with StnCBP to facilitate potato virus Y accumulation through the stress granule-dependent RNA regulatory pathway in potato.Horticulture research · 2022Article
- The TUTase URT1 connects decapping activators and prevents the accumulation of excessively deadenylated mRNAs to avoid siRNA biogenesis.Nature communications · 2021Article
- Functional conservation of EXA1 among diverse plant species for the infection by a family of plant viruses.Scientific reports · 2019Article
- Polysomes, Stress Granules, and Processing Bodies: A Dynamic Triumvirate Controlling Cytoplasmic mRNA Fate and Function.Plant physiology · 2018Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. In addition, necrotrophic pathogens that thrive on dead tissue, take advantage of cell death-triggering mechanisms. Mechanisms by which plants solve this conundrum remain described. Here, we identify PLANT SMY2-TYPE ILE-GYF DOMAIN-CONTAINING PROTEIN 1 (PSIG1) and show that PSIG1 helps to restrict cell death induction during pathogen infection. Inactivation of PSIG1 does not result in spontaneous lesions, and enhanced cell death in psig1 mutants is independent of salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production. Moreover, PSIG1 interacts with SMG7, which plays a role in nonsense-mediated RNA decay (NMD), and the smg7-4 mutant allele mimics the cell death phenotype of the psig1 mutants. Intriguingly, the psig1 mutants display enhanced susceptibility to the hemi-biotrophic bacterial pathogen. These findings point to the existence and importance of the SA- and ROS-independent cell death constraining mechanism as a part of the plant immune system.
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