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#cytoskeletal

2 posts2 participants0 posts today
Public
Rxiv mechanobio

📰 "Magnetic Field-dependent Isotope Effect Supports Radical Pair Mechanism in Tubulin Polymerization"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Dynamics

bioRxiv · Magnetic Field-dependent Isotope Effect Supports Radical Pair Mechanism in Tubulin PolymerizationWeak magnetic fields and isotopes have been shown to influence biological processes; however, the underlying mechanisms remain poorly understood, particularly because the corresponding interaction energies are far below thermal energies, making classical explanations challenging or impossible. Microtubules, dynamic cytoskeletal fibers, offer an ideal system to test weak magnetic field effects due to their self-assembling capabilities, sensitivity to magnetic fields, and their central role in cellular processes. In this study, we use a combination of experiments and simulations to explore how nuclear spin dynamics affect microtubule polymerization by examining interactions between magnesium isotope substitution and weak magnetic fields. Our experiments reveal an isotope-dependent effect, which can be explained via a radical pair mechanism, explicitly arising from nuclear spin properties rather than isotopic mass differences. This nuclear spin-driven isotope effect is notably enhanced under an applied weak magnetic field of approximately 3 mT. Our theoretical model based on radical pairs achieves quantitative agreement with our experimental observations. These results establish a direct connection between quantum spin dynamics and microtubule assembly, providing new insights into how weak magnetic fields influence cellular and biomolecular functions. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Microtubule acetylation is a biomarker of cytoplasmic health during cellular senescence"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Microtubule #Dynamics

bioRxiv · Microtubule acetylation is a biomarker of cytoplasmic health during cellular senescenceCellular senescence is marked by cytoskeletal dysfunction, yet the role of microtubule post-translational modifications (PTMs) remains unclear. We demonstrate that microtubule acetylation increases during drug-induced senescence in human cells and during natural aging in Drosophila. Elevating acetylation via HDAC6 inhibition or αTAT1 overexpression in BEAS-2B cells disrupts anterograde Rab6A vesicle transport, but spares retrograde transport of Rab5 endosomes. Hyperacetylation results in slowed microtubule polymerization and decreased cytoplasmic fluidity, impeding diffusion of micron-sized condensates. These effects are distinct from enhanced detyrosination, and correlate with altered viscoelasticity and resistance to osmotic stress. Modulating cytoplasmic viscosity reciprocally perturbs microtubule dynamics, revealing bidirectional mechanical regulation. Senescent cells phenocopy hyperacetylated cells, exhibiting analogous effects on transport and microtubule polymerization. Our findings establish acetylation as a biomarker for cytoplasmic health and a potential driver of age-related cytoplasmic densification and organelle transport decline, linking microtubule PTMs to biomechanical feedback loops that exacerbate senescence. This work highlights the role of acetylation in bridging cytoskeletal changes to broader aging hallmarks. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Theory of multiscale epithelial mechanics under stretch: from active gels to vertex models"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Mechanical #Mechanics

bioRxiv · Theory of multiscale epithelial mechanics under stretch: from active gels to vertex modelsEpithelial monolayers perform a variety of mechanical functions, which include maintaining a cohesive barrier or developing 3D shapes, while undergoing stretches over a wide range of magnitudes and loading rates. To perform these functions, they rely on a hierarchical organization, which spans molecules, cytoskeletal networks, adhesion complexes and junctional networks up to the tissue scale. While the molecular understanding and ability to manipulate cytoskeletal components within cells is rapidly increasing, how these components integrate to control tissue mechanics is far less understood, partly due to the disconnect between theoretical models of sub-cellular dynamics and those at a tissue scale. To fill this gap, here we propose a formalism bridging active-gel models of the actomyosin cortex and 3D vertex-like models at a tissue scale. We show that this unified framework recapitulates a number of seemingly disconnected epithelial time-dependent phenomenologies, including stress relaxation following stretch/unstretch maneuvers, active flattening after buckling, or nonreciprocal and non-affine pulsatile contractions. We further analyze tissue dynamics probed by a novel experimental setup operating in a pressure-controlled ensemble. Overall, the proposed framework systematically connects sub-cellular cortical dynamics and tissue mechanics, and ties a variety of epithelial phenomenologies to a common sub-cellular origin. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Time irreversibility, entropy production and effective temperature are independently regulated in the actin cortex of living cells"
arxiv.org/abs/2503.17016 #Physics.Bio-Ph #Cytoskeletal #Dynamics #Actin

arXiv logo
arXiv.orgTime irreversibility, entropy production and effective temperature are independently regulated in the actin cortex of living cellsLiving cells exhibit non-equilibrium dynamics emergent from the intricate interplay between molecular motor activity and its viscoelastic cytoskeletal matrix. The deviation from thermal equilibrium can be quantified through frequency-dependent effective temperature or time-reversal symmetry breaking quantified e.g. through the Kullback-Leibler divergence. Here, we investigate the fluctuations of an AFM tip embedded within the active cortex of mitotic human cells with and without perturbations that reduce cortex activity through inhibition of material turnover or motor proteins. While inhibition of motor activity significantly reduces both effective temperature and time irreversibility, inhibited material turnover leaves the effective temperature largely unchanged but lowers the time irreversibility and entropy production rate. Our experimental findings in combination with a minimal model highlight that time irreversibility, effective temperature and entropy production rate can follow opposite trends in active living systems, challenging in particular the validity of effective temperature as a proxy for the distance from thermal equilibrium. Furthermore, we propose that the strength of thermal noise and the occurrence of time-asymmetric deflection spikes in the dynamics of regulated observables are inherently coupled in living systems, revealing a previously unrecognized link between entropy production and time irreversibility.
Public
Rxiv mechanobio

📰 "Flagellar pocket collar biogenesis: Cytoskeletal organization and novel structures in a unicellular parasite"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Dynamics

bioRxiv · Flagellar pocket collar biogenesis: Cytoskeletal organization and novel structures in a unicellular parasiteUnderstanding how cells build and organize their internal structures is a fundamental question in biology, with important implications for human health and disease. Trypanosomes are single-celled flagellated parasites that cause life-threatening diseases in human and animals. Their survival relies on a specialized compartment called the flagellar pocket (FP), which serves as a gateway for nutrient uptake, and immune evasion. The formation and function of the FP are supported by an intricate cytoskeletal structure known as the flagellar pocket collar (FPC). However, the mechanisms underlying its assembly remain poorly understood. In this study, we used cutting-edge ultrastructure expansion microscopy (U-ExM) to investigate FPC biogenesis in Trypanosoma brucei. We mapped the formation of the new microtubule quartet (nMtQ) alongside flagellum growth, providing new insights into its assembly. Additionally, we tracked the localization dynamics of key structural proteins - BILBO1, MORN1, and BILBO2 - during the biogenesis of the FPC and the hook complex (HC). Notably, we identified two previously undetected structures: the proFPC and the transient FPC-interconnecting fibre (FPC-IF), both of which appear to play crucial roles in linking and organizing cellular components during cell division. By uncovering these novel aspects of FPC biogenesis, our study significantly advances the understanding of cytoskeletal organization in trypanosomes and opens new avenues for exploring the functional significance of these structures. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "3D printing cytoskeletal networks: ROS-induced filament severing leads to surge in actin polymerization"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Dynamics

bioRxiv · 3D printing cytoskeletal networks: ROS-induced filament severing leads to surge in actin polymerizationThe cytoskeletal protein actin forms a spatially organized biopolymer network that plays a central role in many cellular processes. Actin filaments continuously assemble and disassemble, enabling cells to rapidly reorganize their cytoskeleton. Filament severing accelerates actin turnover, as both polymerization and depolymerization rates depend on the number of free filament ends - which severing increases. Here, we use light to control actin severing in vitro by locally generating reactive oxygen species (ROS) with photosensitive molecules such as fluorophores. We see that ROS sever actin filaments, which increases actin polymerization in our experiments. However, beyond a certain threshold, excessive severing leads to the disassembly of actin networks. Our experimental data is supported by simulations using a kinetic model of actin polymerization, which helps us understand the underlying dynamics. In cells, ROS are known to regulate the actin cytoskeleton, but the molecular mechanisms are poorly understood. Here we show that, in vitro, ROS directly affect actin reorganization. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Endometriosis and Cytoskeletal Remodeling: The Functional Role of Actin-Binding Proteins"
doi.org/doi:10.3390/cells14050
pubmed.ncbi.nlm.nih.gov/400720
#Cytoskeletal #Dynamics #Actin

MDPIEndometriosis and Cytoskeletal Remodeling: The Functional Role of Actin-Binding ProteinsEndometriosis is a chronic, estrogen-dependent gynecological disorder characterized by the presence of endometrial-like tissue outside the uterine cavity. Despite its prevalence and significant impact on women’s health, the underlying mechanisms driving the invasive and migratory behavior of endometriotic cells remain incompletely understood. Actin-binding proteins (ABPs) play a critical role in cytoskeletal dynamics, regulating processes such as cell migration, adhesion, and invasion, all of which are essential for the progression of endometriosis. This review aims to summarize current knowledge on the involvement of key ABPs in the development and pathophysiology of endometriosis. We discuss how these proteins influence cytoskeletal remodeling, focal adhesion formation, and interactions with the extracellular matrix, contributing to the unique mechanical properties of endometriotic cells. Furthermore, we explore the putative potential of targeting ABPs as a therapeutic strategy to mitigate the invasive phenotype of endometriotic lesions. By elucidating the role of ABPs in endometriosis, this review provides a foundation for future research and innovative treatment approaches.
Public
Rxiv mechanobio

📰 "mTOR regulates Wnt signaling to promote tension-mediated lens vesicle closure"
doi.org/doi:10.1101/2025.02.24
pubmed.ncbi.nlm.nih.gov/400604
#Morphogenesis #Cytoskeletal

bioRxiv · mTOR regulates Wnt signaling to promote tension-mediated lens vesicle closureLens vesicle closure is a pivotal event in ocular morphogenesis, and its disruption underlies Peters anomaly, a leading congenital cause of corneal opacity. Here, we elucidate a mechanistic hierarchy in which mTOR-Wnt signaling orchestrates cytoskeletal tension to drive this process. Conditional ablation of mTOR in the lens ectoderm induces aberrant corneal-lenticular stalk formation and transdifferentiation of the ciliary margin into neural retina. mTOR inhibition suppresses Wnt3 expression, and Wnt3 displayed a similar lens stalk phenotype, positioning mTOR as an upstream regulator of Wnt ligand production. Complete ablation of lens-derived Wnt ligands via deletion of the Wnt transporter Wls exacerbates developmental defects, triggering anterior lens herniation and ciliary margin development failure. Disruption of β-catenin-mediated Wnt signaling or dual deletion of Wnt co-receptors Lrp5/6 in lens ectoderm similarly prevents vesicle closure, recapitulating lens herniation. Strikingly, Rac1 deletion rescues corneal-lenticular stalk phenotypes in mTOR, Wls, and β-catenin mutants, directly linking Wnt effectors to cytoskeletal remodeling. Our findings establish an mTOR-Wnt-Rac1 signaling axis as the core regulator of cytoskeletal tension required for lens vesicle closure. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Tension-Induced Stiffening of Cytoskeletal Components Regulates Cardiomyocyte Contractility"
biorxiv.org/content/10.1101/20 #Cytoskeletal #Mechanical

bioRxiv · Tension-Induced Stiffening of Cytoskeletal Components Regulates Cardiomyocyte ContractilityCardiomyocytes continuously experience mechanical stimuli that regulate their contractile behavior and contribute to overall heart function. Despite the importance of mechanotransduction in cardiac physiology, the mechanisms by which cardiomyocytes integrate external mechanical cues, such as stretch and environmental stiffness, remain poorly understood. In this study, we present a combined theoretical and experimental framework to investigate how strain-induced cytoskeletal stiffening modulates cardiomyocyte contractility and force generation. Our study elucidates that regulating the mechanical tension cardiomyocytes experience in tissue (whether by modulating environmental stiffness, external stretching, or cardiac fibroblast activation) can effectively tune their contractility, with cytoskeletal strain stiffening playing a central role in this mechanotransductive response. ### Competing Interest Statement The authors have declared no competing interest.
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