arXiv subjects

Dipjyoti Das

Publications and source records attributed to Dipjyoti Das.

9 recordsLinked to original sources

arXiv2024

Role of intercellular adhesion in modulating tissue fluidity

Tuning cell rearrangements is essential in collective cell movement that underlies cancer progression, wound repair, and embryonic development. A key question is how tissue material properties and morphology emerge from cellular factors such as cell-cell adhesion. Here, we introduce a two-dimensional active force-based model of tissue monolayers that captures the liquid-to-solid transition exhibited by tissues. Unlike the Vertex and Voronoi models, our model shows that reducing intercellular adhesion in near-confluent tissues leads to spontaneous neighbor exchanges and fluidization. Near the liquid-solid phase boundary, we also found glassy behavior characterized by subdiffusive dynamics, swirling cell motion, and non-Gaussian exponential tails in displacement distributions. These exponential tails collapse onto a single master curve, suggesting a universal 'diffusion length' in the glassy regime. Notably, we demonstrate that structural parameters based on cell shape cannot always distinguish tissue phases due to huge cell shape fluctuations that are not observed in Vertex and Voronoi models. Our general simulation framework streamlines previous approaches by removing many arbitrary features and can reproduce known model behaviors under different conditions, offering potential applications in developmental biology and physiology.

physics.bio-ph↗

arXiv2024

Effects of bursty synthesis in organelle biogenesis

A fundamental question of cell biology is how cells control the number of organelles. The processes of organelle biogenesis, namely de novo synthesis, fission, fusion, and decay, are inherently stochastic, producing cell-to-cell variability in organelle abundance. In addition, experiments suggest that the synthesis of some organelles can be bursty. We thus ask how bursty synthesis impacts intracellular organelle number distribution. We develop an organelle biogenesis model with bursty de novo synthesis by considering geometrically distributed burst sizes. We analytically solve the model in biologically relevant limits and provide exact expressions for the steady-state organelle number distributions and their means and variances. We also present approximate solutions for the whole model, complementing with exact stochastic simulations. We show that bursts generally increase the noise in organelle numbers, producing distinct signatures in noise profiles depending on different mechanisms of organelle biogenesis. We also find different shapes of organelle number distributions, including bimodal distributions in some parameter regimes. Notably, bursty synthesis broadens the parameter regime of observing bimodality compared to the `non-bursty' case. Together, our framework utilizes number fluctuations to elucidate the role of bursty synthesis in producing organelle number heterogeneity in cells.

physics.bio-ph↗

arXiv2019

Cell-to-cell variability in organelle abundance reveals mechanisms of organelle biogenesis

How cells regulate the number of organelles is a fundamental question in cell biology. While decades of experimental work have uncovered four fundamental processes that regulate organelle biogenesis, namely, de novo synthesis, fission, fusion and decay, a comprehensive understanding of how these processes together control organelle abundance remains elusive. Recent fluorescence microscopy experiments allow for the counting of organelles at the single-cell level. These measurements provide information about the cell-to-cell variability in organelle abundance in addition to the mean level. Motivated by such measurements, we build upon a recent study and analyze a general stochastic model of organelle biogenesis. We compute the exact analytical expressions for the probability distribution of organelle numbers, their mean, and variance across a population of single cells. It is shown that different mechanisms of organelle biogenesis lead to distinct signatures in the distribution of organelle numbers which allows us to discriminate between these various mechanisms. By comparing our theory against published data for peroxisome abundance measurements in yeast, we show that a widely believed model of peroxisome biogenesis that involves de novo synthesis, fission, and decay is inadequate in explaining the data. Also, our theory predicts bimodality in certain limits of the model. Overall, the framework developed here can be harnessed to gain mechanistic insights into the process of organelle biogenesis.

q-bio.SC↗

arXiv2016

Sufficient conditions for the additivity of stall forces generated by multiple filaments or motors

Molecular motors and cytoskeletal filaments work collectively most of the time under opposing forces. This opposing force may be due to cargo carried by motors or resistance coming from the cell membrane pressing against the cytoskeletal filaments. Some recent studies have shown that the collective maximum force (stall force) generated by multiple cytoskeletal filaments or molecular motors may not always be just a simple sum of the stall forces of the individual filaments or motors. To understand this excess or deficit in the collective force, we study a broad class of models of both cytoskeletal filaments and molecular motors. We argue that the stall force generated by a group of filaments or motors is additive, that is, the stall force of $N$ number of filaments (motors) is $N$ times the stall force of one filament (motor), when the system is in equilibrium at stall. Conversely, we show that this additive property typically does not hold true when the system is not at equilibrium at stall. We thus present a novel and unified understanding of the existing models exhibiting such non-addivity, and generalise our arguments by developing new models that demonstrate this phenomena. We also propose a quantity similar to thermodynamic efficiency to easily predict this deviation from stall-force additivity for filament and motor collectives.

cond-mat.soft↗

arXiv2014

Collective force generated by multiple biofilaments can exceed the sum of forces due to individual ones

Collective dynamics and force generation by cytoskeletal filaments are crucial in many cellular processes. Investigating growth dynamics of a bundle of N independent cytoskeletal filaments pushing against a wall, we show that chemical switching (ATP/GTP hydrolysis) leads to a collective phenomenon that is currently unknown. Obtaining force-velocity relations for different models that capture chemical switching, we show, analytically and numerically, that the collective stall force of N filaments is greater than N times the stall force of a single filament. Employing an exactly solvable toy model, we analytically prove the above result for N=2. We, further, numerically show the existence of this collective phenomenon, for N>=2, in realistic models (with random and sequential hydrolysis) that simulate actin and microtubule bundle growth. We make quantitative predictions for the excess forces, and argue that this collective effect is related to the non-equilibrium nature of chemical switching.

physics.bio-ph↗

arXiv2014

Force-induced dynamical properties of multiple cytoskeletal filaments are distinct from that of single filaments

How cytoskeletal filaments collectively undergo growth and shrinkage is an intriguing question. Collective properties of multiple bio-filaments (actin or microtubules) undergoing hydrolysis, have not been studied extensively earlier, within simple theoretical frameworks. In this paper, we show that collective properties of multiple filaments under force are very distinct from the properties of a single filament under similar conditions -- these distinctions manifest as follows: (i) the collapse time during collective catastrophe for a multifilament system is much larger than that of a single filament with the same average length, (ii) force-dependence of the cap-size distribution of multiple filaments are quantitatively different from that of single filament, (iii) the diffusion constant associated with the system length fluctuations is distinct for multiple filaments, (iv) switching dynamics of multiple filaments between capped and uncapped states and the fluctuations therein are also distinct. We build a unified picture by establishing interconnections among all these collective phenomena. Additionally, we show that the collapse times during catastrophes can be sharp indicators of collective stall forces exceeding the additive contributions of single filaments.

physics.bio-ph↗

arXiv2012

Giant number fluctuations in microbial ecologies

Statistical fluctuations in population sizes of microbes may be quite large depending on the nature of their underlying stochastic dynamics. For example, the variance of the population size of a microbe undergoing a pure birth process with unlimited resources is proportional to the square of its mean. We refer to such large fluctuations, with the variance growing as square of the mean, as Giant Number Fluctuations (GNF). Luria and Delbruck showed that spontaneous mutation processes in microbial populations exhibit GNF. We explore whether GNF can arise in other microbial ecologies. We study certain simple ecological models evolving via stochastic processes: (i) bi-directional mutation, (ii) lysis-lysogeny of bacteria by bacteriophage, and (iii) horizontal gene transfer (HGT). For the case of bi-directional mutation process, we show analytically exactly that the GNF relationship holds at large times. For the ecological model of bacteria undergoing lysis or lysogeny under viral infection, we show that if the viral population can be experimentally manipulated to stay quasi-stationary, the process of lysogeny maps essentially to one-way mutation process and hence the GNF property of the lysogens follows. Finally, we show that even the process of HGT may map to the mutation process at large times, and thereby exhibits GNF.

q-bio.PE↗

arXiv2012

Broad-tailed force distributions and velocity ordering in a heterogeneous membrane model for collective cell migration

Correlated velocity patterns and associated large length-scale transmission of traction forces have been observed in collective live cell migration as a response to a "wound". We argue that a simple physical model of a force-driven heterogeneous elastic membrane sliding over a viscous substrate can qualitatively explain a few experimentally observed facts: (i) the growth of velocity ordering which spreads from the wound boundary to the interior, (ii) the exponential tails of the traction force distributions, and (iii) the swirling pattern of velocities in the interior of the tissue.

physics.bio-ph↗

arXiv2011

Dynamics of a flexible polymer in planar mixed flow

We present exact spatio-temporal correlation functions of a Rouse polymer chain submerged in a fluid having planar mixed flow, in the steady state. Using these correlators, determination of the time scale distribution functions associated with the first-passage tumbling events is difficult in general; it was done recently in Phys. Rev. Lett.,101, 188301 (2008), for the special case of "simple shear" flow. We show here that the method used in latter paper fails for the general mixed flow problem. We also give many new estimates of the exponent $θ$ associated with the exponential tail of the angular tumbling time distribution in the case of simple shear

cond-mat.stat-mech↗