ArticleCell research2015
Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species.
Article in Cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 122 citations in OpenAlex.
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- Comprehensive identification of glutathione peroxidase (GPX) gene family and effect of GhGPX4 on reactive oxygen species metabolism in cotton.Frontiers in plant science · 2026Article
- A computational analysis of programmed cell death-associated LncRNA signatures in glioma and drug prediction.BMC neurology · 2025Article
- Cellular nitro-oxidative burden and survival through regulated cell death in the plants.Protoplasma · 2025Review
- Chloroplast ATP-dependent metalloprotease FtsH5/VAR1 confers cold-stress tolerance through singlet oxygen and salicylic acid signaling.Plant communications · 2025Article
- Chloroplast precursor protein preClpD overaccumulation triggers multilevel reprogramming of gene expression and a heat shock-like response.Nature communications · 2025Article
- Mitigating drought stress by application of drought-tolerant Bacillus spp. enhanced root architecture, growth, antioxidant and photosynthetic genes expression in sugarcane.Scientific reports · 2025Article
- Effect of membrane rigidification on theFrontiers in plant science · 2025Article
- Effect of Chloroplast ATP Synthase on Reactive Oxygen Species Metabolism in Cotton.International journal of molecular sciences · 2024Article
- Transcriptome analysis to identify genes related to programmed cell death resulted from manipulating of BnaFAH ortholog by CRISPR/Cas9 in Brassica napus.Scientific reports · 2024Article
- Seeing the unseen in characterizing RNA editome during rice endosperm development.Communications biology · 2024Article
- A mitochondrial pentatricopeptide repeat protein enhances cold tolerance by modulating mitochondrial superoxide in rice.Nature communications · 2023Article
- Absence of SICKLE triggers programed cell death by disturbing alternative splicing and decay of mRNAs.Plant physiology · 2023Article
- Rice HEAT SHOCK PROTEIN60-3B maintains male fertility under high temperature by starch granule biogenesis.Plant physiology · 2023Article
- Identification of Candidate QTLs and Genes for Ear Diameter by Multi-Parent Population in Maize.Genes · 2023Article
- ROS accumulation-induced tapetal PCD timing changes leads to microspore abortion in cotton CMS lines.BMC plant biology · 2023Article
- Genome-Wide Association Study Identified Novel SNPs Associated with Chlorophyll Content in Maize.Genes · 2023Article
- Overexpression of an Antioxidant Enzyme APX1 inAntioxidants (Basel, Switzerland) · 2023Article
- Co-regulation of mitochondrial and chloroplast function: Molecular components and mechanisms.Plant communications · 2023Review
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death (PCD) is of fundamental importance to development and defense in animals and plants. In plants, a well-recognized form of PCD is hypersensitive response (HR) triggered by pathogens, which involves the generation of reactive oxygen species (ROS) and other signaling molecules. While the mitochondrion is a master regulator of PCD in animals, the chloroplast is known to regulate PCD in plants. Arabidopsis Mosaic Death 1 (MOD1), an enoyl-acyl carrier protein (ACP) reductase essential for fatty acid biosynthesis in chloroplasts, negatively regulates PCD in Arabidopsis. Here we report that PCD in mod1 results from accumulated ROS and can be suppressed by mutations in mitochondrial complex I components, and that the suppression is confirmed by pharmaceutical inhibition of the complex I-generated ROS. We further show that intact mitochondria are required for full HR and optimum disease resistance to the Pseudomonas syringae bacteria. These findings strongly indicate that the ROS generated in the electron transport chain in mitochondria plays a key role in triggering plant PCD and highlight an important role of the communication between chloroplast and mitochondrion in the control of PCD in plants.
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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.