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A Goldbeter

Publications and source records attributed to A Goldbeter.

80 records · Page 5Linked to original sources
PubMed1975

Control of oscillating glycolysis of yeast by stochastic, periodic, and steady source of substrate: a model and experimental study.

Type and range of entrainment of glycolytic oscillations by a periodic source of substrate are determined experimentally in yeast extracts. Subharmonic entrainment proves the nonlinear nature of the glycolytic oscillator Random variation of the substrate input yields sustained oscillations of irregular waveform and stable period. The results agree with the predictions of an allosteric model for phosphofructokinase (EC 2.7.1.11; ATP:D-fructose-6-phosphate 1-phosphotransferase), which is the enzyme responsible for periodic operation of glycolysis. A comparison between model and experiment in the case of a constant source of substrate further indicates that the oscillatory dynamics of the glycolytic system can satisfactorily be described by the phosphofructokinase model.

Glycolysis↗
PubMed1973

Patterns of spatiotemporal organization in an allosteric enzyme model.

The behavior of a model for an allosteric enzyme oscillator activated by the reaction product is analyzed in the presence of diffusion. When the concentrations of the chemicals are fixed at the boundaries, dynamic dissipative structures are shown to arise in the form of propagating concentration waves. The model is applied to the phosphofructokinase reaction and suggests that a spatiotemporal organization may originate at a macroscopic (supracellular) level from the glycolytic system.

Allosteric Regulation↗
PubMed1972

Dissipative structures for an allosteric model. Application to glycolytic oscillations.

An allosteric model of an open monosubstrate enzyme reaction is analyzed for the case where the enzyme, containing two protomers, is activated by the product. It is shown that this system can lead to instabilities beyond which a new state organized in time or in space (dissipative structure) can be reached. The conditions for both types of instabilities are presented and the occurrence of a temporal structure, consisting of a limit cycle behavior, is determined numerically as a function of the important parameters involved in the system. Sustained oscillations in the product and substrate concentrations are shown to occur for acceptable values of the allosteric and kinetic constants; moreover, they seem to be favored by substrate activation. The model is applied to phosphofructokinase, which is the enzyme chiefly responsible for glycolytic oscillations and which presents the same pattern of regulation as the allosteric enzyme appearing in the model. A qualitative and quantitative agreement is obtained with the experimental observations concerning glycolytic self-oscillations.

Adenosine Monophosphate↗
PubMedDate not supplied

Signal-induced Ca2+ oscillations: properties of a model based on Ca(2+)-induced Ca2+ release.

We consider a simple, minimal model for signal-induced Ca2+ oscillations based on Ca(2+)-induced Ca2+ release. The model takes into account the existence of two pools of intracellular Ca2+, namely, one sensitive to inositol 1,4,5 trisphosphate (InsP3) whose synthesis is elicited by the stimulus, and one insensitive to InsP3. The discharge of the latter pool into the cytosol is activated by cytosolic Ca2+. Oscillations in cytosolic Ca2+ arise in this model either spontaneously or in an appropriate range of external stimulation; these oscillations do not require the concomitant, periodic variation of InsP3. The following properties of the model are reviewed and compared with experimental observations: (a) Control of the frequency of Ca2+ oscillations by the external stimulus or extracellular Ca2+; (b) correlation of latency with period of Ca2+ oscillations obtained at different levels of stimulation; (c) effect of a transient increase in InsP3; (d) phase shift and transient suppression of Ca2+ oscillations by Ca2+ pulses, and (e) propagation of Ca2+ waves. It is shown that on all these counts the model provides a simple, unified explanation for a number of experimental observations in a variety of cell types. The model based on Ca(2+)-induced Ca2+ release can be extended to incorporate variations in the level of InsP3 as well as desensitization of the InsP3 receptor; besides accounting for the phenomena described by the minimal model, the extended model might also account for the occurrence of complex Ca2+ oscillations.

Animals↗
PubMedDate not supplied

Autonomous chaotic behaviour of the slime mould Dictyostelium discoideum predicted by a model for cyclic AMP signalling.

How sustained oscillations lose their periodicity and thus give rise to chaos was first analysed in mathematical models, then observed in chemical systems such as the Belousov-Zhabotinsky reaction where chaos is autonomous because it originates from endogenous kinetic mechanisms. In contrast, chaos can also be obtained by periodically forcing an oscillatory system, as shown, for example, in cardiac cells and yeast glycolysis. Biochemical evidence for autonomous chaos has been obtained both in vitro for the peroxidase reaction and in enzymatic models not based directly on experimental systems. We report here the occurrence of autonomous chaos in a realistic model for the cyclic AMP signalling system of the slime mould Dictyostelium discoideum, based on receptor modification. This model is also capable of bursting, a phenomenon characteristic of some pacemaker neurones such as R15 in Aplysia. Whereas bursting has not been observed in D. discoideum, our model suggests that 'aperiodic signalling' in the mutant Fr17 provides the first example of autonomous chaos occurring spontaneously at the cellular level.

Adenylyl Cyclases↗