Import of phosphatidylserine to and export of phosphatidylethanolamine molecular species from mitochondria

Kainu, Ville; Hermansson, Martin; Hänninen, Satu; Hokynar, Kati; Somerharju, Pentti

doi:10.1016/j.bbalip.2012.11.003

Cited by 46 publications

(71 citation statements)

References 60 publications

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“…Moreover, psd1 Δ yeast have numerous mitochondrial defects even though they retain the ability to synthesize PE via a second Psd enzyme (Psd2p), the CDP-ethanolamine pathway, and Ale1p (Birner et al, 2001; Storey et al, 2001; Trotter and Voelker, 1995). The failure of PE made in the ER to fully support mitochondrial functions in the absence of Psd1p likely reflects its inefficient trafficking into mitochondrial membranes (Birner et al, 2001; Burgermeister et al, 2004; Riekhof et al, 2007b; Shiao et al, 1995) although analysis of the acyl chain composition of PE by mass spectrometry has shown that PE species synthesized by the CDP-ethanolamine pathway are incorporated into the IM in mammalian cells (Bleijerveld et al, 2007; Kainu et al, 2013). Whether the acyl chain composition of PE affects mitochondrial function or if there is a required role in the mitochondrion for Psd1p independent of PE synthesis remain to be investigated.…”

Section: Pe Biosynthesis and Metabolismmentioning

confidence: 99%

Phosphatidylethanolamine Metabolism in Health and Disease

Calzada

Onguka

Claypool

2016

International Review of Cell and Molecular Biology

331

200

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Phosphatidylethanolamine (PE) is the second most abundant glycerophospholipid in eukaryotic cells. The existence of four only partially redundant biochemical pathways that produce PE, highlights the importance of this essential phospholipid. The CDP-ethanolamine and phosphatidylserine decarboxylase pathways occur in different subcellular compartments and are the main sources of PE in cells. Mammalian development fails upon ablation of either pathway. Once made, PE has diverse cellular functions that include serving as a precursor for phosphatidylcholine and a substrate for important posttranslational modifications, influencing membrane topology, and promoting cell and organelle membrane fusion, oxidative phosphorylation, mitochondrial biogenesis, and autophagy. The importance of PE metabolism in mammalian health has recently emerged following its association with Alzheimer's disease, Parkinson's disease, nonalcoholic liver disease, and the virulence of certain pathogenic organisms.

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Section: Pe Biosynthesis and Metabolismmentioning

confidence: 99%

Phosphatidylethanolamine Metabolism in Health and Disease

Calzada

Onguka

Claypool

2016

International Review of Cell and Molecular Biology

331

200

View full text Add to dashboard Cite

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“…Acquity UPLC system equipped with an Acquity BEH-C 18 1.0 × 150 mm column using a solvent gradient described previously [34]. v/v).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…v/v). The choline metabolites were analyzed directly by LC-MS [35], while the ethanolamine and serine metabolites were first converted to dansylated derivatives [36] which were then quantified with LC-MS using SRM [34].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

The PNPLA-family phospholipases involved in glycerophospholipid homeostasis of HeLa cells

Hermansson

Hänninen

Hokynar

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Mammalian cells maintain the glycerophospholipid (GPL) compositions of their membranes nearly constant. To achieve this, GPL synthesis and degradation must be coordinated. There is strong evidence that A-type phospholipases (PLAs) are key players in homeostatic degradation of GPLs, but the identities of the PLAs involved have not been established. However, some members of the Patatin-like phospholipase domain-containing proteins (PNPLAs) have been implicated. Accordingly, we knocked down all the PNPLAs significantly expressed in human HeLa cells using RNA interference and then determined whether the turnover of the major glycerophospholipids is affected by using mass spectrometry and metabolic labeling with stable isotope-labeled precursors. Knockdown of PNPLA9, PNPLA6 or PNPLA4 significantly (30-50%) reduced the turnover of phosphatidylcholine, -ethanolamine and -serine. In a notable contrast, turnover of phosphatidylinositol was not significantly affected by the knockdown of any PNPLA. Depletion of PNPLA9 and PNPLA4 also inhibited G0/G1 to S cell cycle progression, which could thus be regulated by GPL turnover. These results strongly suggest that PNPLA9, -6 and -4 play a key role in GPL turnover and homeostasis in human cells. A hypothetical model suggesting how these enzymes could recognize the relative concentration of the different GPLs is proposed.

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“…Lipid exchange is quantified primarily as PS-to-PE conversion, or as mitochondrial PS content [9]. These strategies require radioisotopes to label phospholipids, which can then be identified and quantified by thin layer chromatography [9] or mass spectroscopy [43,44]. Ca 2+ transfer is more widely used and is typically measured in living cells as increases in mitochondrial Ca 2+ elicited in response to IP 3 [57,58], while the regulation of the PDC is more complex.…”

Section: Bbadis-15-173r2mentioning

confidence: 99%

ER-to-mitochondria miscommunication and metabolic diseases

López-Crisosto

Bravo-Sagua

Rodriguez–Peña

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Eukaryotic cells contain a variety of subcellular organelles, each of which performs unique tasks. Thus follows that in order to coordinate these different intracellular functions, a highly dynamic system of communication must exist between the various compartments. Direct endoplasmic reticulum (ER)-mitochondria communication is facilitated by the physical interaction of their membranes in dedicated structural domains known as mitochondria-associated membranes (MAMs), which facilitate calcium (Ca(2+)) and lipid transfer between organelles and also act as platforms for signaling. Numerous studies have demonstrated the importance of MAM in ensuring correct function of both organelles, and recently MAMs have been implicated in the genesis of various human diseases. Here, we review the salient structural features of interorganellar communication via MAM and discuss the most common experimental techniques employed to assess functionality of these domains. Finally, we will highlight the contribution of MAM to a variety of cellular functions and consider the potential role of MAM in the genesis of metabolic diseases. In doing so, the importance for cell functions of maintaining appropriate communication between ER and mitochondria will be emphasized.

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Import of phosphatidylserine to and export of phosphatidylethanolamine molecular species from mitochondria

Cited by 46 publications

References 60 publications

Phosphatidylethanolamine Metabolism in Health and Disease

Phosphatidylethanolamine Metabolism in Health and Disease

The PNPLA-family phospholipases involved in glycerophospholipid homeostasis of HeLa cells

ER-to-mitochondria miscommunication and metabolic diseases

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