Regulation of phosphatidylcholine biosynthesis under salt stress involves choline kinases in Arabidopsis thaliana

TASSEVA, G

doi:10.1016/s0014-5793(04)00469-7

Cited by 29 publications

(59 citation statements)

References 35 publications

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“…Furthermore, the expression of the PEAMT genes encoding a key enzyme of choline synthesis was induced in lpcat1 lpcat2-2 (Figure 9; see Supplemental Data Set 2 online). These results indicated that the metabolic response of increased de novo PC synthesis involves a series of highly orchestrated molecular steps (Tasseva et al, 2004;Keogh et al, 2009). The weak phenotype of reductions of 18:2 and 18:3 in the TAG of lpcat1 lpcat2-2 also supports the notion that Arabidopsis developing seeds have the capacity to channel 18:1 into PC for desaturation to 18:2 and 18:3 beyond the Lands cycle as well as metabolic plasticity for mobilizing PUFAs into TAG.…”

Section: Discussionmentioning

confidence: 92%

Metabolic Interactions between the Lands Cycle and the Kennedy Pathway of Glycerolipid Synthesis in Arabidopsis Developing Seeds

et al. 2012

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It has been widely accepted that the primary function of the Lands cycle is to provide a route for acyl remodeling to modify fatty acid (FA) composition of phospholipids derived from the Kennedy pathway. Lysophosphatidylcholine acyltransferase (LPCAT) is an evolutionarily conserved key enzyme in the Lands cycle. In this study, we provide direct evidence that the Arabidopsis thaliana LPCATs, LPCAT1 and LPCAT2, participate in the Lands cycle in developing seeds. In spite of a substantially reduced initial rate of nascent FA incorporation into phosphatidylcholine (PC), the PC level in the double mutant lpcat1 lpcat2-2 remained unchanged. LPCAT deficiency triggered a compensatory response of de novo PC synthesis and a concomitant acceleration of PC turnover that were attributable at least in part to PC deacylation. Acyl-CoA profile analysis revealed complicated metabolic alterations rather than merely reduced acyl group shuffling from PC in the mutant. Shifts in FA stereospecific distribution in triacylglycerol of the mutant seed suggested a preferential retention of saturated acyl chains at the stereospecific numbering (sn)-1 position from PC and likely a channeling of lysophosphatidic acid, derived from PC, into the Kennedy pathway. Our study thus illustrates an intricate relationship between the Lands cycle and the Kennedy pathway.

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Section: Discussionmentioning

confidence: 92%

Metabolic Interactions between the Lands Cycle and the Kennedy Pathway of Glycerolipid Synthesis in Arabidopsis Developing Seeds

et al. 2012

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“…The current prevalent view is that the pace-setting enzyme of the Kennedy pathway is not EK, but ECT (43,44). Furthermore overexpression of the EK in mammalian cells does not alter the steady-state levels of PE but only leads to an accumulation of glycerol-phosphoethanolamine (42).…”

Section: The Choline and Ethanolamine Kinasesmentioning

confidence: 99%

“…They also have two ethanolamine-specific kinases: EK1 with negligible CK activity and EK2 with higher affinity for ethanolamine than choline (42). Multiple CKs and a single EK have been identified in Caenorhabditis elegans and Arabidopsis thaliana (43,44), whereas several unicellular eukaryotes have only one member of this enzyme class, probably a dual specificity enzyme (7, 45, 46 and references therein).…”

Section: The Choline and Ethanolamine Kinasesmentioning

confidence: 99%

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The Kennedy pathway—De novo synthesis of phosphatidylethanolamine and phosphatidylcholine

2010

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SummaryThe glycerophospholipids phosphatidylcholine (PC) and phosphatidylethanolamine (PE) account for greater than 50% of the total phospholipid species in eukaryotic membranes and thus play major roles in the structure and function of those membranes. In most eukaryotic cells, PC and PE are synthesized by an aminoalcoholphosphotransferase reaction, which uses sn-1,2-diradylglycerol and either CDP-choline or CDP-ethanolamine, respectively. This is the last step in a biosynthetic pathway known as the Kennedy pathway, so named after Eugene Kennedy who elucidated it over 50 years ago. This review will cover various aspects of the Kennedy pathway including: each of the biosynthetic steps, the functions and roles of the phospholipid products PC and PE, and how the Kennedy pathway has the potential of being a chemotherapeutic target against cancer and various infectious diseases. IUBMBIUBMB Life, 62(6): [414][415][416][417][418][419][420][421][422][423][424][425][426][427][428] 2010

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“…Water-soluble metabolites were obtained from the aqueous supernatant and were fractionated by silica gel TLC developed with MetOH/0.5%NaCl/30%NH 4 OH 50/50/1 (Retention Factors Cho:0.07, Etn:0.16, P-Cho:0.32, P-Etn:0.57, CDP-Cho:0.71, Ser:0.78, and CDP-Etn:0.84) ( 35 ).…”

Section: Syntenic Regions Corresponding To the Genomic Context Of Phomentioning

confidence: 99%

Rodent and nonrodent malaria parasites differ in their phospholipid metabolic pathways

Déchamps

Maynadier

Wein

et al. 2010

Journal of Lipid Research

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Malaria is a disease caused by an intraerythrocytic protozoan parasite of the genus Plasmodium , which is transmitted by dipterans and affects vertebrates such as reptiles, birds, and mammals, including humans (see supplementary Table I). By contrast with other Apicomplexa parasite species that can infect a broad range of metazoans, Plasmodium species have a narrow specifi city range regarding insect and vertebrate hosts ( 1 ). Plasmodium falciparum is, thus, responsible for the most severe form of malaria in humans only. Other species, such as P. vivax , two P. ovale subspecies ( 2 ), P. malariae , and, according to recent reports, P. knowlesi ( 3 ) cause less complicated forms of human malaria. The host specifi city of P. knowlesi is not restricted to humans because it also infects monkeys.The evolutionary history of Plasmodium species has been highly debated, especially the position of P. falciparum , either grouped with avian parasites ( 4, 5 ) or placed as a sister species to other mammalian parasites including rodent parasites. The fi ndings of most recent analyses using three classes of rare genomic changes and mitochondrial RNA genes unambiguously support a mammalian clade and no Abstract Malaria, a disease affecting humans and other animals, is caused by a protist of the genus Plasmodium . At the intraerythrocytic stage, the parasite synthesizes a high amount of phospholipids through a bewildering number of pathways. In the human Plasmodium falciparum species, a plant-like pathway that relies on serine decarboxylase and phosphoethanolamine N-methyltransferase activities diverts host serine to provide additional phosphatidylcholine and phosphatidylethanolamine to the parasite. This feature of parasitic dependence toward its host was investigated in other Plasmodium species. In silico analyses led to the identifi cation of phosphoethanolamine N-methyltransferase gene orthologs in primate and bird parasite genomes. However, the gene was not detected in the rodent P. berghei , P. yoelii , and P. chabaudi species. Biochemical experiments with labeled choline, ethanolamine, and serine showed marked differences in biosynthetic pathways when comparing rodent P. berghei and P. vinckei , and human P. falciparum species. Notably, in both rodent parasites, ethanolamine and serine were not signifi cantly incorporated into phosphatidylcholine, indicating the absence of phosphoethanolamine N-methyltransferase activity. To our knowledge, this is the fi rst study to highlight a crucial difference in phospholipid metabolism between Plasmodium species. The fi ndings should facilitate efforts to develop more rational approaches to identify and evaluate new targets for antimalarial therapy.

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Regulation of phosphatidylcholine biosynthesis under salt stress involves choline kinases in Arabidopsis thaliana

Cited by 29 publications

References 35 publications

Metabolic Interactions between the Lands Cycle and the Kennedy Pathway of Glycerolipid Synthesis in Arabidopsis Developing Seeds

Metabolic Interactions between the Lands Cycle and the Kennedy Pathway of Glycerolipid Synthesis in Arabidopsis Developing Seeds

The Kennedy pathway—De novo synthesis of phosphatidylethanolamine and phosphatidylcholine

Rodent and nonrodent malaria parasites differ in their phospholipid metabolic pathways

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