ArticleFrontiers in plant science2013
Rapid phosphatidic acid accumulation in response to low temperature stress in Arabidopsis is generated through diacylglycerol kinase.
Article in Frontiers in plant science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 1,936 citations in OpenAlex.
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- Light Quantity Impacts Early Response to Cold and Cold Acclimation in Young Leaves of Arabidopsis.Plant, cell & environment · 2025Article
- Concerted transport and phosphorylation of diacylglycerol at ER-PM contact sites regulate phospholipid dynamics during stress.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Ergosterol-induced immune response in barley involves phosphorylation of phosphatidylinositol phosphate metabolic enzymes and activation of diterpene biosynthesis.The New phytologist · 2025Article
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- Heat shock factor ZmHsf17 positively regulates phosphatidic acid phosphohydrolase ZmPAH1 and enhances maize thermotolerance.Journal of experimental botany · 2025Article
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- Drought and heat stress mediated activation of lipid signaling in plants: a critical review.Frontiers in plant science · 2023Review
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- Effect of Drought Stress on Degradation and Remodeling of Membrane Lipids inFoods (Basel, Switzerland) · 2022Article
- The Effect of Cold Stress on the Root-Specific Lipidome of Two Wheat Varieties with Contrasting Cold Tolerance.Plants (Basel, Switzerland) · 2022Article
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- Full-length transcriptome sequencing reveals the molecular mechanism of potato seedlings responding to low-temperature.BMC plant biology · 2022Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Phosphatidic acid (PtdOH) is emerging as an important signaling lipid in abiotic stress responses in plants. The effect of cold stress was monitored using (32)P-labeled seedlings and leaf discs of Arabidopsis thaliana. Low, non-freezing temperatures were found to trigger a very rapid (32)P-PtdOH increase, peaking within 2 and 5 min, respectively. In principle, PtdOH can be generated through three different pathways, i.e., (1) via de novo phospholipid biosynthesis (through acylation of lyso-PtdOH), (2) via phospholipase D hydrolysis of structural phospholipids, or (3) via phosphorylation of diacylglycerol (DAG) by DAG kinase (DGK). Using a differential (32)P-labeling protocol and a PLD-transphosphatidylation assay, evidence is provided that the rapid (32)P-PtdOH response was primarily generated through DGK. A simultaneous decrease in the levels of (32)P-PtdInsP, correlating in time, temperature dependency, and magnitude with the increase in (32)P-PtdOH, suggested that a PtdInsP-hydrolyzing PLC generated the DAG in this reaction. Testing T-DNA insertion lines available for the seven DGK genes, revealed no clear changes in (32)P-PtdOH responses, suggesting functional redundancy. Similarly, known cold-stress mutants were analyzed to investigate whether the PtdOH response acted downstream of the respective gene products. The hos1, los1, and fry1 mutants were found to exhibit normal PtdOH responses. Slight changes were found for ice1, snow1, and the overexpression line Super-ICE1, however, this was not cold-specific and likely due to pleiotropic effects. A tentative model illustrating direct cold effects on phospholipid metabolism is presented.
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