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Register a new userCurvature and torsion in growing actin networks
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Intracellular pathogens such as Listeria monocytogenes and Rickettsia rickettsii move within a host cell by polymerizing a comet-tail of actin fibers that ultimately pushes the cell forward. This dense network of cross-linked actin polymers typically exhibits a striking curvature that causes bacteria to move in gently looping paths. Theoretically, tail curvature has been linked to details of motility by considering force and torque balances from a finite number of polymerizing filaments. Here we track beads coated with a prokaryotic activator of actin polymerization in three dimensions to directly quantify the curvature and torsion of bead motility paths. We find that bead paths are more likely to have low rather than high curvature at any given time. Furthermore, path curvature changes very slowly in time, with an autocorrelation decay time of 200 seconds. Paths with a small radius of curvature, therefore, remain so for an extended period resulting in loops when confined to two dimensions. When allowed to explore a 3D space, path loops are less evident. Finally, we quantify the torsion in the bead paths and show that beads do not exhibit a significant left- or right-handed bias to their motion in 3D. These results suggest that paths of actin-propelled objects may be attributed to slow changes in curvature rather than a fixed torque.
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The growth of several biological tissues is known to be controlled in part by local geometrical features, such as the curvature of the tissue interface. This control leads to changes in tissue shape that in turn can affect the tissues evolution. Understanding the cellular basis of this control is highly significant for bioscaffold tissue engineering, the evolution of bone microarchitecture, wound healing, and tumour growth. While previous models have proposed geometrical relationships between tissue growth and curvature, the role of cell density and cell vigor remains poorly understood. We propose a cell-based mathematical model of tissue growth to investigate the systematic influence of curvature on the collective crowding or spreading of tissue-synthesising cells induced by changes in local tissue surface area during the motion of the interface. Depending on the strength of diffusive damping, the model exhibits complex growth patterns such as undulating motion, efficient smoothing of irregularities, and the generation of cusps. We compare this model with in-vitro experiments of tissue deposition in bioscaffolds of different geometries. By accounting for the depletion of active cells, the model is able to capture both smoothing of initial substrate geometry and tissue deposition slowdown as observed experimentally.
We study the motion of oil drops propelled by actin polymerization in cell extracts. Drops deform and acquire a pear-like shape under the action of the elastic stresses exerted by the actin comet. We solve this free boundary problem and calculate the drop shape taking into account the elasticity of the actin gel and the variation of the polymerization velocity with normal stress. The pressure balance on the liquid drop imposes a zero propulsive force if gradients in surface tension or internal pressure are not taken into account. Quantitative parameters of actin polymerization are obtained by fitting theory to experiment.
Muscle uses Ca2+ as a messenger to control contraction and relies on ATP to maintain the intracellular Ca2+ homeostasis. Mitochondria are the major sub-cellular organelle of ATP production. With a negative inner membrane potential, mitochondria take up Ca2+ from their surroundings, a process called mitochondrial Ca2+ uptake. Under physiological conditions, Ca2+ uptake into mitochondria promotes ATP production. Excessive uptake causes mitochondrial Ca2+ overload, which activates downstream adverse responses leading to cell dysfunction. Moreover, mitochondrial Ca2+ uptake could shape spatio-temporal patterns of intracellular Ca2+ signaling. Malfunction of mitochondrial Ca2+ uptake is implicated in muscle degeneration. Unlike non-excitable cells, mitochondria in muscle cells experience dramatic changes of intracellular Ca2+ levels. Besides the sudden elevation of Ca2+ level induced by action potentials, Ca2+ transients in muscle cells can be as short as a few milliseconds during a single twitch or as long as minutes during tetanic contraction, which raises the question whether mitochondrial Ca2+ uptake is fast and big enough to shape intracellular Ca2+ signaling during excitation-contraction coupling and creates technical challenges for quantification of the dynamic changes of Ca2+ inside mitochondria. This review focuses on characterization of mitochondrial Ca2+ uptake in skeletal muscle and its role in muscle physiology and diseases.
In eukaryotic genes the protein coding sequence is split into several fragments, the exons, separated by non-coding DNA stretches, the introns. Prokaryotes do not have introns in their genome. We report the calculations of stability domains of actin genes for various organisms in the animal, plant and fungi kingdoms. Actin genes have been chosen because they have been highly conserved during evolution. In these genes all introns were removed so as to mimic ancient genes at the time of the early eukaryotic development, i.e. before introns insertion. Common stability boundaries are found in evolutionary distant organisms, which implies that these boundaries date from the early origin of eukaryotes. In general boundaries correspond with introns positions of vertebrates and other animals actins, but not much for plants and fungi. The sharpest boundary is found in a locus where fungi, algae and animals have introns in positions separated by one nucleotide only, which identifies a hot-spot for insertion. These results suggest that some introns may have been incorporated into the genomes through a thermodynamic driven mechanism, in agreement with previous observations on human genes. They also suggest a different mechanism for introns insertion in plants and animals.
Bacteria such as Escherichia coli move about in a series of runs and tumbles: while a run state (straight motion) entails all the flagellar motors spinning in counterclockwise mode, a tumble is caused by a shift in the state of one or more motors to clockwise spinning mode. In the presence of an attractant gradient in the environment, runs in the favourable direction are extended, and this results in a net drift of the organism in the direction of the gradient. The underlying signal transduction mechanism produces directed motion through a bi-lobed response function which relates the clockwise bias of the flagellar motor to temporal changes in the attractant concentration. The two lobes (positive and negative) of the response function are separated by a time interval of $sim 1$s, such that the bacterium effectively compares the concentration at two different positions in space and responds accordingly. We present here a novel path-integral method which allows us to address this problem in the most general way possible, including multi-step CW-CCW transitions, directional persistence and power-law waiting time distributions. The method allows us to calculate quantities such as the effective diffusion coefficient and drift velocity, in a power series expansion in the attractant gradient. Explicit results in the lowest order in the expansion are presented for specific models, which, wherever applicable, agree with the known results. New results for gamma-distributed run interval distributions are also presented.
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