Cell cycle progression is an essential regulatory component of phospholipid metabolism and membrane homeostasis

Sánchez-Álvarez, Miguel; Zhang, Qifeng; Finger, Fabian; Wakelam, Michael J.O.; Bakal, Chris

doi:10.1098/rsob.150093

Cited by 41 publications

(39 citation statements)

References 57 publications

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“…Recent studies have indicated the role of SREBP-1 in controlling cell cycle progression, including G 0 /G 1 and G 2 /M phases (Bengoechea-Alonso et al, 2005;Motallebipour et al, 2009;Sanchez-Alvarez et al, 2015). Recent studies have indicated the role of SREBP-1 in controlling cell cycle progression, including G 0 /G 1 and G 2 /M phases (Bengoechea-Alonso et al, 2005;Motallebipour et al, 2009;Sanchez-Alvarez et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…FASN is one of two key enzymes that transfer carbon flux from glycolysis into lipid synthesis. A recent study has further indicated that SREBP-1 activity might be regulated by mTORC1 signaling (Porstmann et al, 2008;Sanchez-Alvarez, Zhang, Finger, Wakelam, & Bakal, 2015). The signaling of mammalian target of rapamycin complex 1 (mTORC1), which is composed of mTOR kinase and its regulatory-associated proteinraptor, also functions as a well-known energy sensor and regulates cell proliferation and growth (Sarbassov, Ali, & Sabatini, 2005;Wullschleger, Loewith, & Hall, 2006).…”

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confidence: 99%

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Glucose adsorption to chitosan membranes increases proliferation of human chondrocyte via mammalian target of rapamycin complex 1 and sterol regulatory element‐binding protein‐1 signaling

Chang

Huang

Cheng

et al. 2017

Journal Cellular Physiology

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Osteoarthritis (OA) is currently still an irreversible degenerative disease of the articular cartilage. Recent, dextrose (d-glucose) intraarticular injection prolotherapy for OA patients has been reported to benefit the chondrogenic stimulation of damaged cartilage. However, the detailed mechanism of glucose's effect on cartilage repair remains unclear. Chitosan, a naturally derived polysaccharide, has recently been investigated as a surgical or dental dressing to control breeding. Therefore, in this study, glucose was adsorbed to chitosan membranes (CTS-Glc), and the study aimed to investigate whether CTS-Glc complex membranes could regulate the proliferation of human OA chondrocytes and to explore the underlying mechanism. Human OA and SW1353 chondrocytes were used in this study. The experiments involving the transfection of cells used SW1353 chondrocytes. A specific inhibitor and siRNAs were used to investigate the mechanism underlying the CTS-Glc-regulated proliferation of human chondrocytes. We found that CTS-Glc significantly increased the proliferation of both human OA and SW1353 chondrocytes comparable to glucose- or chitosan-only stimulation. The role of mammalian target of rapamycin complex 1 (mTORC1) signaling, including mTOR, raptor, and S6k proteins, has been demonstrated in the regulation of CTS-Glc-increased human chondrocyte proliferation. mTORC1 signaling increased the expression levels of maturated SREBP-1 and FASN and then induced the expressions of cell cycle regulators, that is, cyclin D, cyclin-dependent kinase-4 and -6 in human chondrocytes. This study elucidates the detailed mechanism behind the effect of CTS-Glc complex membranes in promoting chondrocyte proliferation and proposes a possible clinical application of the CTS-Glc complex in the dextrose intraarticular injection of OA prolotherapy in the future to attenuate the pain and discomfort of OA patients.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Glucose adsorption to chitosan membranes increases proliferation of human chondrocyte via mammalian target of rapamycin complex 1 and sterol regulatory element‐binding protein‐1 signaling

Chang

Huang

Cheng

et al. 2017

Journal Cellular Physiology

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“…Intriguingly, it has recently been reported that mammalian cells remodel their membrane lipid composition during the cell cycle, and these periodic changes are important for proper cell-cycle progression. [50][51][52] Curiously, the mitotic defects of the Dcbf11 and cut6-621 mutants were alleviated when cells were grown in the minimal EMM medium (Fig. 4B and ref.…”

Section: Discussionmentioning

confidence: 99%

CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast

et al. 2016

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For every eukaryotic cell to grow and divide, intricately coordinated action of numerous proteins is required to ensure proper cell-cycle progression. The fission yeast Schizosaccharomyces pombe has been instrumental in elucidating the fundamental principles of cell-cycle control. Mutations in S. pombe 'cut' (cell untimely torn) genes cause failed coordination between cell and nuclear division, resulting in catastrophic mitosis. Deletion of cbf11, a fission yeast CSL transcription factor gene, triggers a 'cut' phenotype, but the precise role of Cbf11 in promoting mitotic fidelity is not known. We report that Cbf11 directly activates the transcription of the acetyl-coenzyme A carboxylase gene cut6, and the biotin uptake/ biosynthesis genes vht1 and bio2, with the former 2 implicated in mitotic fidelity. Cbf11 binds to a canonical, metazoan-like CSL response element (GTGGGAA) in the cut6 promoter. Expression of Cbf11 target genes shows apparent oscillations during the cell cycle using temperature-sensitive cdc25-22 and cdc10-M17 block-release experiments, but not with other synchronization methods. The penetrance of catastrophic mitosis in cbf11 and cut6 mutants is nutrient-dependent. We also show that drastic decrease in biotin availability arrests cell proliferation but does not cause mitotic defects. Taken together, our results raise the possibility that CSL proteins play conserved roles in regulating cell-cycle progression, and they could guide experiments into mitotic CSL functions in mammals.

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“…However, those mechanisms are far too slow to acutely regulate the GPL composition without energy wasting fluctuations (hysteresis). Those “coarse” mechanisms rather come into play when a change in GPL composition is required as, for example, during mitosis, cell differentiation or by altered cellular environment . In principle, protein phosphorylation (or other modifications) could play a role in acute regulation of GPL compositions since those processes can take place rapidly and can influence protein activity .…”

Section: Introductionmentioning

confidence: 99%

Hypothesis: Chemical activity regulates and coordinates the processes maintaining glycerophospholipid homeostasis in mammalian cells

2020

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Mammalian cells maintain the complex glycerophospholipid (GPL) class compositions of their various membranes within close limits because this is essential to their well‐being or viability. Surprisingly, however, it is still not understood how those compositions are maintained except that GPL synthesis and degradation are closely coordinated. Here, we hypothesize that abrupt changes in the chemical activity of the individual GPL classes coordinate synthesis and degradation as well other the homeostatic processes. We have previously proposed that only a limited number of “allowed” or “optimal” GPL class compositions exist in cellular membranes because those compositions are energetically more favorable than others, that is, they represent local free energy minima (Somerharju et al 2009, Biochim. Biophys. Acta 1788, 12‐23). This model, however, could not satisfactorily explain how the “optimal” compositions are sensed by the key homeostatic enzymes, that is, rate‐limiting synthetizing enzymes and homeostatic phospholipases. We now hypothesize that when the mole fraction of a GPL class exceeds an optimal value, its chemical activity abruptly increases which (a) increases its propensity to efflux from the membrane thus making it susceptible for hydrolysis by homeostatic phospholipases; (b) increases its potency to inhibit its own biosynthesis via a feedback mechanism; (c) enhances its conversion to another glycerophospholipid class via a novel process termed “head group remodeling” or (d) enhances its translocation to other subcellular membranes. In summary, abrupt change in the chemical activity of the individual GPL classes is proposed to regulate and coordinate those four processes maintaining GPL class homeostasis in mammalian cells.

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Cell cycle progression is an essential regulatory component of phospholipid metabolism and membrane homeostasis

Cited by 41 publications

References 57 publications

Glucose adsorption to chitosan membranes increases proliferation of human chondrocyte via mammalian target of rapamycin complex 1 and sterol regulatory element‐binding protein‐1 signaling

Glucose adsorption to chitosan membranes increases proliferation of human chondrocyte via mammalian target of rapamycin complex 1 and sterol regulatory element‐binding protein‐1 signaling

CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast

Hypothesis: Chemical activity regulates and coordinates the processes maintaining glycerophospholipid homeostasis in mammalian cells

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