Biology subjects

Banerjee, D. S.

Publications and source records attributed to Banerjee, D. S..

8 recordsLinked to original sources

bioRxiv2025

Excitability and travelling waves in renewable active matter

Activity and renewability are distinctive features of living matter, and constitute a new class of materials that we term renewable active matter. A striking example is the cell cytoskeleton, where myosin filaments bind to the actin meshwork, apply contractile stresses and undergo continual stress/strain dependent turnover, thus acting as both force generators and sensors. As a consequence of nonreciprocity, arising from the independence of action and response, such living matter exhibits unusual mechanical properties like, segregation without attraction, fragility and force chains. Here we show that the interplay between activity and turnover gives rise to mechanical excitability in the form of travelling waves and pulses, and spatiotemporal chaos. We provide a systematic study of the nucleation, movement and shape of the travelling pulse, and present a boundary layer analysis to establish the existence of homoclinic orbits. Our analytical results are supported by detailed numerical analysis of the governing partial differential equations. This study has implications for the observed mechanical excitability in a variety of cellular contexts such as in isolated adherent cells and confluent cells within tissues.

biophysics↗

bioRxiv2024

Interplay of condensate material properties and chromatin heterogeneity governs nuclear condensate ripening

Nuclear condensates play many important roles in chromatin functions, but how cells regulate their nucleation and growth within the complex nuclear environment is not well understood. Here, we report how condensate properties and chromatin mechanics dictate condensate growth dynamics in the nucleus. We induced condensates with distinct properties using different proteins in human cell nuclei and monitored their growth. We revealed two key physical mechanisms that underlie droplet growth: diffusion-driven or ripening-dominated growth. To explain the experimental observations, we developed a quantitative theory that uncovers the mechanical role of chromatin and condensate material properties in regulating condensate growth in a heterogeneous environment. By fitting our theory to experimental data, we find that condensate surface tension is critical in determining whether condensates undergo elastic or Ostwald ripening. Our model also predicts that chromatin heterogeneity can influence condensate nucleation and growth, which we validated by experimentally perturbing the chromatin organization and controlling condensate nucleation. By combining quantitative experimentation with theoretical modeling, our work elucidates how condensate surface tension and chromatin heterogeneity govern nuclear condensate ripening, implying that cells can control both condensate properties and the chromatin organization to regulate condensate growth in the nucleus.

biophysics↗

bioRxiv2024

Contractile to extensile transitions and mechanical adaptability enabled by activity in cytoskeletal structures

Cytoskeletal network architecture is crucial in determining emergent morphology and dynamics, particularly in processes like stress fiber nucleation, where cells respond to mechanical cues. However, a clear understanding of the connection between architecture, dynamics, and mechanical response remains lacking. In this study, we investigate how self-assembled cytoskeletal structures respond to external mechanical perturbations, focusing on filament and crosslinker mixtures in two dimensions. Using agent-based models complemented by coarse-grained thermodynamic analysis, we reveal how molecular motor activity enables cytoskeletal structures to robustly adapt to changing mechanical conditions. Our simulations demonstrate that under tensile forces, self-assembled active asters transform into bundle-like structures, reminiscent of de novo stress fiber formation in living cells, while pre-existing active bundles elongate further in a reproducible and regulated manner. In contrast, passive assemblies exhibit no such qualitative morphological reorganization, highlighting the critical role of activity in mechanical adaptation. We derive a simple relation approximating active stress as a function of average relative motor alignment, a measure of mesoscopic architecture, which allows us to predict changes in stress characteristics in response to mechanical perturbations with or without morphological reorganization. Our results demonstrate how mesoscopic architecture and motor activity work in tandem to enable robust morphological and mechanical adaptation in cytoskeletal structures, providing insight into cellular mechanosensing and stress fiber formation.

biophysics↗

bioRxiv2024

Growth-induced collective bending and kinetic trapping of cytoskeletal filaments

Growth and turnover of actin filaments play a crucial role in the construction and maintenance of actin networks within cells. Actin filament growth occurs within limited space and finite subunit resources in the actin cortex. To understand how filament growth shapes the emergent architecture of actin networks, we developed a minimal agent-based model coupling filament mechanics and growth in a limiting subunit pool. We find that rapid filament growth induces kinetic trapping of highly bent actin filaments. Such collective bending patterns are long-lived, organized around nematic defects, and arises from competition between filament polymerization and bending elasticity. The stability of nematic defects and the extent of kinetic trapping are amplified by an increase in the abundance of the actin pool and by crosslinking the network. These findings suggest that kinetic trapping is a robust consequence of growth in crowded environments, providing a route to program shape memory in actin networks.

biophysics↗

bioRxiv2023

Catalytic growth in a shared enzyme pool ensures robust control of centrosome size

Accurate regulation of centrosome size is essential for ensuring error-free cell division, and dysregulation of centrosome size has been linked to various pathologies, including developmental defects and cancer. While a universally accepted model for centrosome size regulation is lacking, prior theoretical and experimental works suggest a centrosome growth model involving autocatalytic assembly of the pericentriolar material. Here we show that the autocatalytic assembly model fails to explain the attainment of equal centrosome sizes, which is crucial for error-free cell division. Incorporating latest experimental findings into the molecular mechanisms governing centrosome assembly, we introduce a new quantitative theory for centrosome growth involving catalytic assembly within a shared pool of enzymes. Our model successfully achieves robust size equality between maturing centrosome pairs, mirroring cooperative growth dynamics observed in experiments. To validate our theoretical predictions, we compare them with available experimental data and demonstrate the broad applicability of the catalytic growth model across different organisms, which exhibit distinct growth dynamics and size scaling characteristics.

cell biology↗

bioRxiv2021

Emergence and maintenance of different sized actin filaments in a common pool of building blocks

Actin is one of the key structural components of the eukaryotic cytoskeleton that regulates cellular architecture and mechanical properties. Dynamic regulation of actin filament length and organization is essential for the control of many physiological processes including cell adhesion, motility and division. While previous studies have mostly focused on the mechanisms controlling the mean length of individual actin filaments, it remains poorly understood how distinct actin filament populations in cells maintain different lengths using the same set of molecular building blocks. Here we develop a theoretical model for the length regulation of multiple actin filaments by nucleation and growth rate modulation by actin binding proteins in a limiting pool of monomers. We first show that spontaneous nucleation of actin filaments naturally leads to heterogeneities in filament length distribution. We then investigate the effects of filament growth inhibition by capping proteins and growth promotion by formin proteins on filament length distribution. We find that filament length heterogeneity can be increased by growth inhibition, whereas growth promoters do not significantly affect length heterogeneity. Interestingly, a competition between filament growth inhibitors and growth promoters can give rise to bimodal filament length distribution as well as a highly heterogeneous length distribution with large statistical dispersion. We quantitatively predict how heterogeneity in actin filament length can be modulated by tuning F-actin nucleation and growth rates in order to create distinct filament subpopulations with different lengths. SIGNIFICANCEActin filaments organize into different functional network architectures within eukaryotic cells. To maintain distinct actin network architectures, it is essential to regulate the lengths of actin filaments. While the mechanisms controlling the lengths of individual actin filaments have been extensively studied, the regulation of length heterogeneity in actin filament populations is not well understood. Here we show that the modulation of actin filament growth and nucleation rates by actin binding proteins can regulate actin length distribution and create distinct sub-populations with different lengths. In particular, by tuning concentrations of formin, profilin and capping proteins, various aspects of actin filament length distribution can be controlled. Insights gained from our results may have significant implications for the regulation of actin filament length heterogeneity and architecture within a cell.

biophysics↗

bioRxiv2020

Segmentation and analysis of mother machine data: SAM

Time-lapse imaging of bacteria growing in micro-channels in a controlled environment has been instrumental in studying the single cell dynamics of bacterial growth. This kind of a microfluidic setup with growth chambers is popularly known as mother machine [1]. In a typical experiment with such a set-up, bacterial growth can be studied for numerous generations with high resolution and temporal precision using image processing. However, as in any other experiment involving imaging, the image data from a typical mother machine experiment has considerable intensity fluctuations, cell intrusion, cell overlapping, filamentation etc. The large amount of data produced in such experiments makes it hard for manual analysis and correction of such unwanted aberrations. We have developed a modular code for segmentation and analysis of mother machine data (SAM) for rod shaped bacteria where we can detect such aberrations and correctly treat them without manual supervision. We track cumulative cell size and use an adaptive segmentation method to avoid faulty detection of cell division. SAM is currently written and compiled using MATLAB. It is fast ([~] 15 min/GB of image) and can be efficiently coupled with shell scripting to process large amount of data with systematic creation of output file structures and graphical results. It has been tested for many different experimental data and is publicly available in Github.

systems biology↗

bioRxiv2020

Size regulation of multiple organelles competing for a shared subunit pool

How cells regulate the size of intracellular structures and organelles, despite continuous turnover in their component parts, is a longstanding question. Recent experiments suggest that size control of many intracellular assemblies is achieved through the depletion of a limiting subunit pool in the cytoplasm. While the limiting pool model ensures organelle size scaling with cell size, it does not provide a mechanism for robust size control of multiple co-existing structures. Here we propose a kinetic theory for size regulation of multiple structures that are assembled from a shared pool of subunits. We demonstrate that a negative feedback between the growth rate and the size of individual structures underlies size regulation of a wide variety of intracellular assemblies, from cytoskeletal filaments to three-dimensional organelles such as centrosomes and the nucleus. We identify the feedback motifs for size control in these structures, based on known molecular interactions, and quantitatively compare our theory with available experimental data. Furthermore, we show that a positive feedback between structure size and growth rate can lead to bistable size distributions arising from autocatalytic growth. In the limit of high subunit concentration, autocatalytic growth of multiple structures leads to stochastic selection of a single structure, elucidating a mechanism for polarity establishment.

biophysics↗