Phospholipid metabolism of 3T3 mouse fibroblasts after serum stimulation and through the Gl and S cell cycle phases : incorporation and disappearance of 32P

Dubois, C.; Rampini, C

doi:10.1016/s0300-9084(79)80448-4

Cited by 8 publications

(5 citation statements)

References 17 publications

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“…The correlations with the earlier observed modulations in membrane fluidity and in lateral mobility of membrane lipids (de Laat et al, 1980) suggest a relation to structural and physicochemical changes in the plasma membrane. This view is supported by the proposed insertion of phospholipids into the plasma membrane around mitosis (Dubois and Rampini, 1978;Stein and Berestecky, 1975;Scott et al, 1971;Bluemink and de Laat, 1977) and the reported control of cation permeability by the membrane lipid composition (Chen et al, 1978).…”

Section: Discussionmentioning

confidence: 92%

“…The lateral mobility o f membrane proteins was also modulated during the cell cycle (de Laat et al, 1980) in partial association with these changes. Incorporation of phospholipids in 3T3 cells occurs particularly in G1 phase (Dubois and Rampini, 1978). The membrane protein composition has been shown to be cell cycle-dependent in HeLa cells (Johnson et al, 1975).…”

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confidence: 99%

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Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle

Boonstra

Mummery

Tertoolen

et al. 1981

Journal Cellular Physiology

103

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Cation transport and membrane potential were studied during the cell cycle of neuroblastoma cells (clone Neuro-2A) to investigate the role of these parameters in growth regulation. The cells were synchronized by selective detachment of mitotic cells. The membrane potential and intracellular K+ activity were measured with conventional and K+-selective microelectrodes respectively. Both the membrane potential and K+ activity were high in mitosis, decreased to half maximal in G1 phase, and rose again during S phase. K+ efflux across the plasma membrane was studied with 42K+ as a radioactive tracer using a washing method for cells grown in monolayer and a continuous efflux method for mitotic cells in suspension. The intracellular K+ content and unidirectional K+ efflux rate obtained from these measurements showed modulations during the cell cycle similar to those of the membrane potential. Using equations of electrodiffusion theory the membrane permeabilities to K+ and Na+ were calculated. These permeabilities were high in mitosis, decreased rapidly in G1 phase and increased during S phase, followed by a transient decrease in G2 phase. A rapid increase was observed between G2 phase and the next mitosis. A similar pattern was obtained for the K+ conductance. K+ resistance changes during the cell cycle were similar to changes in the specific membrane resistance, measured by microelectrodes, except for the early cell cycle phases (mitosis and G1). These studies clearly demonstrate large modulations of the passive membrane permeability properties during the cell cycle. These modulations can be correlated with physicochemical membrane variations during the cell cycle, such as membrane fluidity and lateral mobility of lipids.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle

Boonstra

Mummery

Tertoolen

et al. 1981

Journal Cellular Physiology

103

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“…This was in contrast with other phospholipids, turnover of which remained relatively constant during the same period. Somewhat different results were described by Dubois & Rampini (1978), who reported that PtdIns turnover is stimulated during GI and S Abbreviations used: Ptdlns, phosphatidylinositol; PtdIns4P, phosphatidylinositol 4-phosphate; Ptdlns(4,5)P2, phosphatidylinositol 4,5bisphosphate; P-PI, polyphosphoinositide; PtdCho, phosphatidylcholine; PtdEtn, phosphatidylethanolamine; PtdSer, phosphatidylserine; PtdOH, phosphatidic acid; InsP, inositol monophosphate; InsP2, inositol bisphosphate; InsP3, inositol trisphosphate; DMEM, Dulbecco's modification of Eagle's medium. * Present address: CIBA-Geigy Pharmaceuticals, Wimblehurst Road, Horsham, West Sussex RH12 4AB, U.K. t Present address: Parke-Davis Research Unit, Addenbrooke's Hospital Site, Hills Road, Cambridge CB2 2QB, U.K. t To whom reprint requests should be addressed.…”

Section: Introductionmentioning

confidence: 79%

Phospholipid turnover during cell-cycle traverse in synchronous Chinese-hamster ovary cells. Mitogenesis without phosphoinositide breakdown

Tones

Sharif

Hawthorne

1988

Biochemical Journal

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The turnover of phospholipids was investigated in quiescent serum-starved Chinese-hamster ovary (CHO-K1) cells stimulated to progress through the cell cycle by the addition of dialysed bovine serum. A variety of radiolabelling techniques were employed to study the rapid effects of serum on phospholipids and later events during G1 and S phases of the cell cycle. Pulse-labelling studies using [32P]Pi revealed that there was a stimulation of the synthesis rate of all phospholipids investigated during the initial few hours after serum addition. The greatest stimulation (20-fold) was observed in phosphatidylcholine, and the smallest in the polyphosphoinositides (PPIs). Mock stimulation with serum-free medium caused a similar increase in PPI turnover, but little or no effect on turnover of other phospholipids. This effect could be accounted for by a stimulation of the turnover of cellular ATP pools increasing [32P]ATP specific radioactivity. Late G1 and S phases were associated with a decrease in the rate of synthesis of all phospholipids. Phosphatidic acid was the only phospholipid whose labelling fell below that in mock-stimulated cells during the period of the cell cycle. Stimulation of serum-starved cells that had been prelabelled with myo-[2-3H]inositol caused no change in the amounts of inositol trisphosphate, but both serum-stimulated and mock-stimulated cells exhibited similar small decreases in both inositol bisphosphate and inositol monophosphate, of approx. 30% after 30 s. When cells were serum-stimulated in the presence of 10 mM-Li+, there was no increase in the size of the total inositol phosphate pool. We conclude that mitogenic stimulation and cell-cycle traverse cause profound and complex effects on phospholipid turnover in CHO-K1 cells, but there is no evidence for a role of inositol lipid turnover in the proliferative response to serum in this cell line.

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“…A key experiment was to follow the pattern of phospholipid accumulation through the second cell cycle following synchronization to convincingly distinguish that membrane phospholipid acquisition was a cell cycle-regulated process rather than a growth factor-triggered event that took several hours to initiate (12). The distribution of major phospholipid classes in whole cells was essentially constant throughout the cell cycle in NIH fibroblasts (11). Likewise, the content of PtdIns, PtdIns-P, and PtdIns-P 2 was relatively constant during the cell cycle (23), although specific changes have been observed in the nuclear compartment (see below).…”

Section: S Phasementioning

confidence: 99%

Cell Cycle Regulation of Membrane Phospholipid Metabolism

Jackowski

1996

Journal of Biological Chemistry

197

169

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This review focuses on the phospholipid metabolism regulated by the cell cycle. Phospholipids are the major cellular constituents required for the assembly of biological membranes, and cells must double their phospholipid mass to form daughter cells. It seems reasonable that this event should coincide with the synthesis of other cellular components such as DNA, stable RNA, etc.; however, the biochemical mechanisms that coordinate macromolecular and bulk membrane phospholipid production are largely unknown. The importance of these regulatory processes to cell physiology is obvious. Discordant regulation of phospholipid accumulation by only a few percent per cell cycle would rapidly result in cells with either a large excess or deficit of membrane surface leading to abnormalities in cell size and/or intracellular lipid accumulation. Thus, stringent control mechanisms must be in place to keep the phospholipid content in tune with the cell cycle. This discussion will explore the state of our knowledge in cultured mammalian cell systems, although cell cycle-regulated phospholipid accumulation occurs in lower eukaryotes such as Saccharomyces cerevisiae (1) and Caulobacter crescentus (2). This review is limited to a discussion of events that are directly tied to the cell cycle. Phospholipid metabolism in response to mitogenic stimulation will not be addressed as these biochemical events are generally associated with the G 0 to G 1 transition and are ligand-regulated rather than being orchestrated by the cell cycle. G 1 PhaseThe G 1 phase of the cell cycle is characterized as having a high rate of membrane phospholipid turnover. Increased incorporation of label into phospholipids and elevated levels of intracellular soluble phospholipid precursors were noted after the mitogenic stimulation of cells (3, 4), although these studies did not address whether the increase in labeling represented net phospholipid synthesis or enhanced phospholipid turnover (5-11). Jackowski (12) examined both synthesis and degradation in a macrophage cell line using a double label experiment and attributed the increase in choline incorporation into PtdCho 1 during G 1 (4) to rapid PtdCho turnover (12). Importantly, the rate of PtdCho degradation decreased by an order of magnitude in S phase and then accelerated again as the cells entered the next G 1 period, thereby establishing that PtdCho turnover in G 1 was associated with the cell cycle and not a property of the G 0 to G 1 transition (12). The cessation of PtdCho degradation in S phase is likely an important contributor to the net accumulation of phospholipid during this time; however, nothing is known about the biochemical processes that govern the periodicity of PtdCho turnover. PtdCho turnover may be an important aspect of phospholipid metabolism during G 1 that is necessary, and in some cases, sufficient for entry into S phase. PtdCho hydrolysis by phospholipase C and/or D pathways is triggered by a wide array of agonists (9), and both exogenous bacterial PtdCho phospholipase C (13) and...

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Phospholipid metabolism of 3T3 mouse fibroblasts after serum stimulation and through the Gl and S cell cycle phases : incorporation and disappearance of 32P

Cited by 8 publications

References 17 publications

Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle

Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle

Phospholipid turnover during cell-cycle traverse in synchronous Chinese-hamster ovary cells. Mitogenesis without phosphoinositide breakdown

Cell Cycle Regulation of Membrane Phospholipid Metabolism

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Phospholipid metabolism of 3T3 mouse fibroblasts after serum stimulation and through the Gl and S cell cycle phases : incorporation and disappearance of 32P

Cited by 8 publications

References 17 publications

Cation transport and growth regulation in neuroblastoma cells. Modulations of K+ transport and electrical membrane properties during the cell cycle

Cation transport and growth regulation in neuroblastoma cells. Modulations of K+ transport and electrical membrane properties during the cell cycle

Phospholipid turnover during cell-cycle traverse in synchronous Chinese-hamster ovary cells. Mitogenesis without phosphoinositide breakdown

Cell Cycle Regulation of Membrane Phospholipid Metabolism

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Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle

Cation transport and growth regulation in neuroblastoma cells. Modulations of K⁺ transport and electrical membrane properties during the cell cycle