ArticleThe Journal of biological chemistry2015
Altered Lipid Synthesis by Lack of Yeast Pah1 Phosphatidate Phosphatase Reduces Chronological Life Span.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Pooled it
- Crosstalk between protein kinases Pho85-Pho80 and Rim11 regulates Pah1 phosphatidate phosphatase function in lipid synthesis.The Journal of biological chemistry · 2026Article
- Phospholipid biosynthesis modulates nucleotide metabolism and reductive capacity.Nature chemical biology · 2025Article
- Sugar accelerates chronological aging in yeast via ceramides.Cell stress · 2025Review
- Architecture and function of yeast phosphatidate phosphatase Pah1 domains/regions.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024Review
- The PAH1-encoded phosphatidate phosphatase of Yarrowia lipolytica differentially affects gene expression and lipid biosynthesis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024Article
- Boosting Geranyl Diphosphate Synthesis for Linalool Production in Engineered Yarrowia lipolytica.Applied biochemistry and biotechnology · 2024Article
- A dynamic actin cytoskeleton is required to prevent constitutive VDAC-dependent MAPK signalling and aberrant lipid homeostasis.iScience · 2023Article
- Improving therapeutic protein secretion in the probiotic yeast Saccharomyces boulardii using a multifactorial engineering approach.Microbial cell factories · 2023Article
- Phosphorylation-mediated regulation of the Nem1-Spo7/Pah1 phosphatase cascade in yeast lipid synthesis.Advances in biological regulation · 2022Review
- The MoPah1 phosphatidate phosphatase is involved in lipid metabolism, development, and pathogenesis in Magnaporthe oryzae.Molecular plant pathology · 2022Article
- Reengineering of 7-dehydrocholesterol biosynthesis inFrontiers in microbiology · 2022Article
- Metabolic engineering strategies for de novo biosynthesis of sterols and steroids in yeast.Bioresources and bioprocessing · 2021Review
- HJournal of fungi (Basel, Switzerland) · 2021Article
- Engineering of Saccharomyces cerevisiae for the accumulation of high amounts of triacylglycerol.Microbial cell factories · 2021Article
- A review of phosphatidate phosphatase assays.Journal of lipid research · 2020Review
- The Spo7 sequence LLI is required for Nem1-Spo7/Pah1 phosphatase cascade function in yeast lipid metabolism.The Journal of biological chemistry · 2020Article
- Yeast phosphatidic acid phosphatase Pah1 hops and scoots along the membrane phospholipid bilayer.Journal of lipid research · 2020Article
- Phosphatidate-mediated regulation of lipid synthesis at the nuclear/endoplasmic reticulum membrane.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- High production of triterpenoids inBiotechnology for biofuels · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In Saccharomyces cerevisiae, Pah1 phosphatidate phosphatase, which catalyzes the dephosphorylation of phosphatidate to yield diacylglycerol, plays a crucial role in the synthesis of the storage lipid triacylglycerol. This evolutionarily conserved enzyme also plays a negative regulatory role in controlling de novo membrane phospholipid synthesis through its consumption of phosphatidate. We found that the pah1Δ mutant was defective in the utilization of non-fermentable carbon sources but not in oxidative phosphorylation; the mutant did not exhibit major changes in oxygen consumption rate, mitochondrial membrane potential, F1F0-ATP synthase activity, or gross mitochondrial morphology. The pah1Δ mutant contained an almost normal complement of major mitochondrial phospholipids with some alterations in molecular species. Although oxidative phosphorylation was not compromised in the pah1Δ mutant, the cellular levels of ATP in quiescent cells were reduced by 2-fold, inversely correlating with a 4-fold increase in membrane phospholipids. In addition, the quiescent pah1Δ mutant cells had 3-fold higher levels of mitochondrial superoxide and cellular lipid hydroperoxides, had reduced activities of superoxide dismutase 2 and catalase, and were hypersensitive to hydrogen peroxide. Consequently, the pah1Δ mutant had a shortened chronological life span. In addition, the loss of Tsa1 thioredoxin peroxidase caused a synthetic growth defect with the pah1Δ mutation. The shortened chronological life span of the pah1Δ mutant along with its growth defect on non-fermentable carbon sources and hypersensitivity to hydrogen peroxide was suppressed by the loss of Dgk1 diacylglycerol kinase, indicating that the underpinning of pah1Δ mutant defects was the excess synthesis of membrane phospholipids.
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