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M J Saxton

Publications and source records attributed to M J Saxton.

11 recordsLinked to original sources
PubMed1992

Gaps in the erythrocyte membrane skeleton: a stretched net model.

The geometry of spectrin-free regions in the erythrocyte membrane skeleton is modeled using Monte Carlo calculations for an incomplete triangular lattice of entropy springs under tension. Intact springs correspond to normal spectrin molecules, and cut springs correspond to spectrin that is missing or unable to associate normally. As springs are cut and the network is allowed to relax to mechanical equilibrium, gaps in the network appear. Geometrical properties of these gaps are obtained as a function of the fraction of springs cut. The most important property modeled is the area of the largest spectrin-free region; this area increases approximately exponentially as the fraction of normal spectrin decreases from 100% to approximately 50%. The effect of these gaps on lateral diffusion and vesiculation is discussed.

Erythrocyte Membrane↗
PubMed1992

Lateral diffusion and aggregation. A Monte Carlo study.

Aggregation in a lipid bilayer is modeled as cluster-cluster aggregation on a square lattice. In the model, clusters carry out a random walk on the lattice, with a diffusion coefficient inversely proportional to mass. On contact, they adhere with a prescribed probability, rigidly and irreversibly. Monte Carlo calculations show that, as expected, rotational diffusion of the aggregating species is highly sensitive to the initial stages of aggregation. Lateral diffusion of an inert tracer obstructed by the aggregate is a sensitive probe of the later stages of aggregation. Cluster-cluster aggregates are much more effective barriers to lateral diffusion of an inert tracer than the same area fraction of random point obstacles is, but random point obstacles are more effective barriers than the same area fraction of compact obstacles. The effectiveness of aggregates as obstacles is discussed in terms of particle-particle correlation functions and fractal dimensions. Results are applicable to aggregation of membrane proteins, and at least qualitatively to aggregation of gel-phase lipid during lateral phase separation.

Diffusion↗
PubMed1991

Oligosaccharide signaling in plants. Specificity of oligouronide-enhanced plasma membrane protein phosphorylation.

The in vitro phosphorylation by [gamma-32P]ATP of a 34-kDa plasma membrane-associated protein (pp34) from tomato and potato is strongly enhanced in the presence of alpha-1,4-D-polygalacturonic acid (PGA) fragments (Farmer, E. E., Pearce, G., and Ryan, C. A. (1989) Proc. Natl. Acad. Sci. U. S. A. 86, 1539-1542) that activate the expression of defensive and developmental genes in plant tissues. [gamma-35S]ATP, but not [gamma-35S]GTP, has now been found to strongly label pp34 in the presence of the PGA fragments. PGA-enhanced phosphorylation of pp34 is at one or more threonine residue(s) and therefore is the product of a serine/threonine kinase. alpha-1,4-L-Polyguluronic acid (PGU) enhances thiophosphorylation of pp34, but is less effective than PGA. beta-1,4-D-Polymannuronic acid (PMA) is inactive. In vivo synthesis of proteinase inhibitors in tomato leaves in response to PGA, PGU, and PMA parallels enhancing activities in in vitro phosphorylation assays. The minimum oligogalacturonide lengths that enhance in vitro thiophosphorylation of pp34 are about 14-15 residues, which are near the minimum sizes of uronides required to elicit a variety of localized defensive and developmental responses in plants. The lengths of biologically active galacturonic acid oligomers are of the same length that form strong intermolecular complexes in solution with Ca2+. Uronide-Ca2+ complexes are proposed to be the active molecular species that initiate the signal transduction pathways regulating uronide-responsive genes.

Adenosine Triphosphate↗
PubMed1990

The membrane skeleton of erythrocytes: models of its effect on lateral diffusion.

The membrane skeleton, a network of structural proteins attached to the cytoplasmic surface of the plasma membrane, hinders lateral diffusion of integral proteins. 2. In some types of cells, such as epithelial cells and nerve cells, the obstruction of lateral diffusion by the membrane skeleton is one of the mechanisms by which proteins are localized to domains on the cell surface. 3. The effect of the membrane skeleton on lateral diffusion may involve steric hindrance, transient binding or both. Three pictures of the effect are reviewed, the discrete barrier model, the continuous barrier model and the transient binding model. 4. Experiments to distinguish the models are discussed.

Animals↗
PubMed1990

Lateral diffusion in a mixture of mobile and immobile particles. A Monte Carlo study.

The lateral diffusion coefficient for mixtures of mobile and immobile particles is obtained from Monte Carlo calculations of random walks by mobile tracers in the presence of immobile obstacles on a triangular lattice. The diffusion coefficient of the mobile species is obtained as a function of the area fractions of mobile and immobile species. The results are applied to diffusion of band 3 in the erythrocyte membrane, and indicate that obstruction of diffusion of mobile band 3 by band 3 and glycophorin attached to the membrane skeleton is not sufficient to explain the observed diffusion coefficient.

Animals↗
PubMed1990

The membrane skeleton of erythrocytes. A percolation model.

The spectrin network on the cytoplasmic surface of the erythrocyte membrane is modeled as a triangular lattice of spectrin tetramers. This network obstructs lateral diffusion of proteins and provides mechanical reinforcement to the membrane. These effects are treated in a systematic and unified manner in terms of a percolation model. The diffusion coefficient is obtained as a function of the fraction of normal spectrin tetramers for both static and fluctuating barriers. The elasticity of the network is calculated as a function of the fraction of normal spectrin and the ratio of bending to stretching energies. For static barriers, elasticity and lateral diffusion are incompatible: if a network is connected enough to be elastic, it is connected enough to block long-range lateral diffusion. The elasticity and the force required for mechanical breakdown go to zero at the percolation threshold; experimental evidence suggests the existence of a stability threshold at or near the percolation threshold. The model is qualitatively applicable to other cells with membrane skeletons, such as epithelial cells, in which localization of membrane proteins is essential to differentiation.

Algorithms↗
PubMed1989

Concentration effects on reactions in membranes: rhodopsin and transducin.

The reaction rate of two laterally-diffusing species in a biological membrane shows a maximum at some concentration of reactants, because an increase in the concentration of reactants tends to increase the reaction rate by the law of mass action but decreases the diffusion rate of the reactants. The activation of transducin by rhodopsin in the disk membrane of the rod outer segment is described in terms of a steady-state diffusion model with concentration-dependent diffusion coefficients. The optimum concentrations of reactants are obtained from contour plots of the reaction rate as a function of rhodopsin and transducin concentrations, and the sensitivity of the results to the assumed values of the variables is examined. To determine whether the observed concentrations are in fact those yielding the maximum reaction rate, several variables must be known more accurately.

Diffusion↗
PubMed1989

Lateral diffusion in an archipelago. Distance dependence of the diffusion coefficient.

An understanding of the distance dependence of the lateral diffusion coefficient is useful in comparing the results of diffusion measurements made over different length scales, and in analyzing the kinetics of mobile redox carriers in organelles. A distance-dependent, concentration-dependent diffusion coefficient is defined, and it is evaluated by Monte Carlo calculations of a random walk by mobile point tracers in the presence of immobile obstacles on a triangular lattice, representing the diffusion of a lipid or a small protein in the presence of immobile membrane proteins. This work confirms and extends the milling crowd model of Eisinger, J., J. Flores, and W. P. Petersen (1986. Biophys J. 49:987-1001). Similar calculations for diffusion of mobile particles interacting by a hard-core repulsion yield the distance dependence of the self-diffusion coefficient. An expression for the range of short-range diffusion is obtained, and the distance scales for various diffusion measurements are summarized.

Diffusion↗
PubMed1989

The spectrin network as a barrier to lateral diffusion in erythrocytes. A percolation analysis.

The spectrin network on the cytoplasmic surface of an erythrocyte can be modeled as a triangular lattice of spectrin tetramers (Tsuji, A., and S. Ohnishi, 1986. Biochemistry. 25:6133-6139). The tetramers act as barriers to protein diffusion, while dissociated dimer pairs, single dimers, and missing tetramers do not. Diffusion in the presence of these barriers is shown to be equivalent to bond percolation on the honeycomb lattice. Monte Carlo calculations for this system then yield the relative diffusion constant of a mobile integral protein as a function of the fraction of spectrin tetramers. At high concentrations of spectrin tetramer, long-range diffusion is blocked, but short-range diffusion is still possible. Monte Carlo calculations yield the average distance over which short-range diffusion can occur, as a function of the fraction of spectrin tetramers. Applications to erythrocyte development and hereditary hemolytic anemia are discussed.

Algorithms↗
PubMed1987

Lateral diffusion in an archipelago. The effect of mobile obstacles.

Lateral diffusion of mobile proteins and lipids (tracers) in a membrane is hindered by the presence of proteins (obstacles) in the membrane. If the obstacles are immobile, their effect may be described by percolation theory, which states that the long-range diffusion constant of the tracers goes to zero when the area fraction of obstacles is greater than the percolation threshold. If the obstacles are themselves mobile, the diffusion constant of the tracers depends on the area fraction of obstacles and the relative jump rate of tracers and obstacles. This paper presents Monte Carlo calculations of diffusion constants on square and triangular lattices as a function of the concentration of obstacles and the relative jump rate. The diffusion constant for particles of various sizes is also obtained. Calculated values of the concentration-dependent diffusion constant are compared with observed values for gramicidin and bacteriorhodopsin. The effect of the proteins as inert obstacles is significant, but other factors, such as protein-protein interactions and perturbation of lipid viscosity by proteins, are of comparable importance. Potential applications include the diffusion of proteins at high concentrations (such as rhodopsin in rod outer segments), the modulation of diffusion by release of membrane proteins from cytoskeletal attachment, and the diffusion of mobile redox carriers in mitochondria, chloroplasts, and endoplasmic reticulum.

Cell Membrane↗