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Lack of phosphatidate phosphatase causes reduced chronological life span through increased energy expenditure and oxidative stress
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Park, Yeonhee. Lack of phosphatidate phosphatase causes reduced chronological life span through increased energy expenditure and oxidative stress. Retrieved from https://doi.org/doi:10.7282/T3P27102

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TitleLack of phosphatidate phosphatase causes reduced chronological life span through increased energy expenditure and oxidative stress
NamePark, Yeonhee (author); Carman, George M (chair); Han, Gil-Soo (internal member); Quadro, Loredana (internal member); Gillies, Peter (outside member); Rutgers University; Graduate School - New Brunswick
Date Created2015
Other Date2015-05 (degree)
SubjectFood Science, Lipids--Metabolism, Phosphatidate phosphatase
Extent1 online resource (xiii, 129 p. : ill.)
DescriptionIn Saccharomyces cerevisiae, Pah1 phosphatidate phosphatase, which catalyzes the dephosphorylation of phosphatidic acid (PA) to yield diacylglycerol (DAG), plays a major role in the synthesis of the storage lipid triacylglycerol. The evolutionarily conserved enzyme also regulates de novo phospholipid synthesis by controlling the level of PA, a precursor of membrane phospholipids. In this work, we showed that the pah1Δ mutant is defective in growth on non-fermentable carbon sources. Despite its apparent phenotype for respiratory deficiency, the pah1 mutant exhibited typical mitochondrial attributes, and even had an elevated mitochondrial membrane potential at the post-diauxic shift. Although oxidative phosphorylation was not compromised, the cellular levels of ATP in quiescent pah1 mutant cells were reduced by two-fold, which correlated with a four-fold increase in membrane phospholipids. Furthermore, the quiescent mutant cells exhibited three-fold elevations in mitochondrial superoxide and cellular lipid hydroperoxides, and acute sensitivity to hydrogen peroxide. Consequently, the pah1 mutant had a shortened chronological life span. This phenotype, along with the inability to grow on non-fermentable carbon sources and sensitivity to hydrogen peroxide was complemented by loss of the DGK1-encoded DAG kinase indicating that the underpinning of pah1 defects in quiescence was the imbalance of PA/DAG. These results indicate that Pah1 PAP plays a crucial role in energy conservation and chronological life span through its regulation of lipid synthesis.
NotePh.D.
NoteIncludes bibliographical references
Noteby Yeonhee Park
Genretheses, ETD doctoral
Persistent URLhttps://doi.org/doi:10.7282/T3P27102
Languageeng
CollectionGraduate School - New Brunswick Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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