Dataset Information

Cortical factor feedback model for cellular locomotion and cytofission.

ABSTRACT: Eukaryotic cells can move spontaneously without being guided by external cues. For such spontaneous movements, a variety of different modes have been observed, including the amoeboid-like locomotion with protrusion of multiple pseudopods, the keratocyte-like locomotion with a widely spread lamellipodium, cell division with two daughter cells crawling in opposite directions, and fragmentations of a cell to multiple pieces. Mutagenesis studies have revealed that cells exhibit these modes depending on which genes are deficient, suggesting that seemingly different modes are the manifestation of a common mechanism to regulate cell motion. In this paper, we propose a hypothesis that the positive feedback mechanism working through the inhomogeneous distribution of regulatory proteins underlies this variety of cell locomotion and cytofission. In this hypothesis, a set of regulatory proteins, which we call cortical factors, suppress actin polymerization. These suppressing factors are diluted at the extending front and accumulated at the retracting rear of cell, which establishes a cellular polarity and enhances the cell motility, leading to the further accumulation of cortical factors at the rear. Stochastic simulation of cell movement shows that the positive feedback mechanism of cortical factors stabilizes or destabilizes modes of movement and determines the cell migration pattern. The model predicts that the pattern is selected by changing the rate of formation of the actin-filament network or the threshold to initiate the network formation.

SUBMITTER: Nishimura SI

PROVIDER: S-EPMC2645504 | biostudies-literature | 2009 Mar

REPOSITORIES: biostudies-literature

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Cortical factor feedback model for cellular locomotion and cytofission.

Nishimura Shin I SI Ueda Masahiro M Sasai Masaki M

PLoS computational biology 20090313 3

Eukaryotic cells can move spontaneously without being guided by external cues. For such spontaneous movements, a variety of different modes have been observed, including the amoeboid-like locomotion with protrusion of multiple pseudopods, the keratocyte-like locomotion with a widely spread lamellipodium, cell division with two daughter cells crawling in opposite directions, and fragmentations of a cell to multiple pieces. Mutagenesis studies have revealed that cells exhibit these modes depending ...[more]

PMID: 19282961

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Project description:The mechanisms underlying an effective propagation of high intensity information over a background of irregular firing and response latency in cognitive processes remain unclear. Here we propose a SSCCPI circuit to address this issue. We hypothesize that when a high-intensity thalamic input triggers synchronous spike events (SSEs), dense spikes are scattered to many receiving neurons within a cortical column in layer IV, many sparse spike trains are propagated in parallel along minicolumns at a substantially high speed and finally integrated into an output spike train toward or in layer Va. We derive the sufficient conditions for an effective (fast, reliable, and precise) SSCCPI circuit: (i) SSEs are asynchronous (near synchronous); (ii) cortical columns prevent both repeatedly triggering SSEs and incorrectly synaptic connections between adjacent columns; and (iii) the propagator in interneurons is temporally complete fidelity and reliable. We encode the membrane potential responses to stimuli using the non-linear autoregressive integrated process derived by applying Newton's second law to stochastic resilience systems. We introduce a multithreshold decoder to correct encoding errors. Evidence supporting an effective SSCCPI circuit includes that for the condition, (i) time delay enhances SSEs, suggesting that response latency induces SSEs in high-intensity stimuli; irregular firing causes asynchronous SSEs; asynchronous SSEs relate to healthy neurons; and rigorous SSEs relate to brain disorders. For the condition (ii) neurons within a given minicolumn are stereotypically interconnected in the vertical dimension, which prevents repeated triggering SSEs and ensures signal parallel propagation; columnar segregation avoids incorrect synaptic connections between adjacent columns; and signal propagation across layers overwhelmingly prefers columnar direction. For the condition (iii), accumulating experimental evidence supports temporal transfer precision with millisecond fidelity and reliability in interneurons; homeostasis supports a stable fixed-point encoder by regulating changes to synaptic size, synaptic strength, and ion channel function in the membrane; together all-or-none modulation, active backpropagation, additive effects of graded potentials, and response variability functionally support the multithreshold decoder; our simulations demonstrate that the encoder-decoder is temporally complete fidelity and reliable in special intervals contained within the stable fixed-point range. Hence, the SSCCPI circuit provides a possible mechanism of effective signal propagation in cortical networks.

Dataset Information

Cortical factor feedback model for cellular locomotion and cytofission.

Publications

Cortical factor feedback model for cellular locomotion and cytofission.

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