Biology subjects

Mogilner, A.

Publications and source records attributed to Mogilner, A..

At least 19 recordsLinked to original sources

bioRxiv2026

Hierarchy of spindle forces in prometaphase

Dramatic movements characterize rapid assembly of mitotic spindle in prometaphase: chromosomes congress to the spindle equator, while spindle poles segregate rapidly elongating the spindle. Direct biophysical measurements of forces driving these movements are lacking, but the forces could be learned from the rapid pole and chromosome movements. We analyzed 3D trajectories of chromosomes and spindle poles in the wild-type and PRC1-depleted cells during early prometaphase and reconstructed the spindle forces. This analysis posits that (i) chromosomes do not interact with each other, except for a short-range steric repulsion, (ii) effective pole-chromosome forces are repulsive at short and attractive at long distances, (iii) dominant forces of spindle poles segregation are interpolar in origin. The important implication of these results is that the pole-pole segregation is robust, largely insensitive to regional variations inside the cell and to complex process of chromosome congression.

biophysics↗

bioRxiv2026

Hierarchical binding of cognition to action in the human basal ganglia-thalamic circuit

Flexible behavior requires binding actions to their underlying cognitive variables, yet classical basal ganglia models emphasize a serial architecture where striatal action selection precedes a pallidothalamic motor gate. We tested this framework by recording single-neuron activity across the human pallidothalamic circuit while participants reported perceptual decisions with confidence-weighted reaching movements. Neurons in globus pallidus externus and internus, subthalamic nucleus, and motor thalamus exhibited sharp activity increases at movement onset that persisted through execution and feedback. Choice and confidence were continuously encoded before, during, and after movement. Population decoding revealed a transformation along the circuit, from dynamic upstream representations to stable, low-dimensional representations downstream, particularly in motor thalamus. After feedback, outcome signals emerged selectively in subthalamic nucleus and motor thalamus. In motor thalamus, confidence and outcome converged into a representation consistent with unsigned reward prediction error. These findings redefine the human pallidothalamic circuit as an interface that binds decision, action, and evaluation during behavior.

neuroscience↗

bioRxiv2026

Reconstructing Actin Dynamics of the Leading Edge from Observational Data

Mesenchymal cell migration starts with the protrusion of the cells leading edge, enabled by the branching growth of the actin network. Two crucial molecular players in protrusion are actin filaments and the Arp2/3 protein complex, the branching agent. Traditionally, protrusion models are intuited from several perturbative experiments. Recent multiplex microscopy imaging data promise to drastically change this paradigm by providing measurements of naturally fluctuating densities of key proteins at the leading edge of unperturbed cells. We report the first attempt to reconstruct the mechanistic protrusion model from such data. We analyze fluctuations of F-actin and Arp2/3 densities and cell edge velocity using phase space and regression analysis to reconstruct linearized stochastic actin-Arp2/3-velocity coupled dynamics. We then build a nonlinear partial differential equation model of these dynamics based on previous knowledge of this system and parsimony. The resulting model recovers the rates of reactions and mechanical and transport processes in the lamellipodium from a single non-perturbative experiment. The model posits that the only essential nonlinearities in the lamellipodial dynamics stem from the retrograde flow of F-actin. The model suggests that the protrusion is dominated by a damped oscillatory cycle resulting from a combination of positive feedback from Arp2/3 to protrusion velocity and negative feedback from F-actin to the velocity. Significance statementTraditionally, models of intracellular mechanochemistry are intuited from perturbative experiments. Multiplex microscopy imaging changes this by providing measurements of naturally fluctuating densities of key proteins in unperturbed cells. We use such data to reconstruct a mechanistic model of cell leading edge. We build equations for actin system and edge velocity using data, previous knowledge and parsimony. The resulting model recovers the rates of reactions and mechanical and transport processes at the leading edge. The model suggests that the protrusion is dominated by a damped oscillatory cycle resulting from a combination of positive feedback from Arp2/3 to protrusion velocity and negative feedback from F-actin to the velocity.

biophysics↗

bioRxiv2025

Non-uniform filament turnover and mechanically-driven contractility and bundle formation in disordered actomyosin networks

Bundles of actin filaments with similar positions and orientations commonly occur in cytoskeletal networks. We use mathematical modelling and simulation to investigate how filament turnover and mechanics influence contractility and bundle formation in disordered actomyosin networks. Using a two-dimensional agent-based model for an actomyosin network, we investigate four simplified models for filament turnover: uniform, biased, branching, and treadmilling. With no turnover, over time contractility decreases and bundle formation increases, and networks eventually form stationary patterns that cannot contract. Introducing turnover allows contractility to persist longer compared to the no-turnover scenario. Uniform turnover, where new filaments have random positions and orientations, disrupts bundle formation and enables persistent contractility. In biased turnover, branching, and treadmilling, the positions and orientations of new filaments depend on the existing network. These non-uniform turnover models increase bundle formation compared to uniform turnover, while still allowing long-term contractility. Branching at 70{degrees} disrupts bundle formation to enable prolonged contractility, whereas filament treadmilling disrupts the trade-off between bundle formation and contractility. Biased turnover places new filaments near existing ones, which promotes bundle formation but is less effective at maintaining contractility. We also varied mechanical factors in our simulations, especially filament bending flexibility and protein friction, which enhance bundle formation and contractility, respectively. Our results suggest that variations in turnover and mechanics might allow cells to tune contractility and bundle formation in disordered actomyosin networks.

biophysics↗

bioRxiv2025

Ordering from the edge: Chiral multicellular pattern formation directed by actin self-organisation in cells

The mechanisms underlying both the establishment of mirror symmetry and deviations from it in development of bilateral multicellular organisms remain insufficiently understood. Actin cytoskeletons of individual cells exhibit intrinsic chirality, and a strong correlation exists between single-cell actin fibres chiral organisation and the collective alignment of cells confined to rectangular adhesive islands (2D-microtissues). Here, we demonstrate how multicellular chiral patterns can be inferred from the chiral behaviour of actin fibres in individual cells. By analysing chiral actin systems in cells with elliptical and semi-circular shapes, representing inner and boundary positions within 2D-microtissues, we defined the rules of chiral motile behaviour and formulated two models of cell alignment: (i) chiral rotation of inner cells and (ii) chiral tilting of boundary cells relative to island edges. In both models, neighbouring cells are also mutually aligned. Systematic variation of island area and aspect ratio, combined with dynamic observations, revealed the primary role of boundary cells. Chiral order first emerged at tissue boundaries and then propagated inward. This outside-in mechanism also explains why mirror-symmetric cell groups are difficult to achieve with uniformly chiral cells, but can be obtained either by reversing chirality in one subgroup or by enlarging the microtissue to minimise boundary influence.

biophysics↗

bioRxiv2025

The kinetochore corona orchestrates chromosome congression through transient microtubule interactions

For proper segregation of chromosomes and successful cytokinesis, chromosomes must first congress - gather in a tight plate near the spindle equator. Molecular mechanism(s) of congression are not fully understood. Here we combine live cell microscopy, perturbations of microtubule motor activities, correlative light/electron microscopy, and computational modeling, to quantitatively characterize the early-prometaphase movements that bring the scattered chromosomes to the equator in human RPE1 cells. We find that the early-prometaphase movements are predominantly directed toward the spindle center and not the spindle poles. Centromere velocity of the centripetal movements is not constant with centromeres moving faster at larger distances from the spindle center. We also detect that numerous short microtubules appear at kinetochores at the earliest stages of spindle assembly and prior to chromosome congression. Computational modeling reveals that a mechanism based on brief, stochastic, minus-end directed interactions between the short microtubules protruding from the kinetochores and long appropriately curved microtubules within the spindle accurately predicts the observed distance-velocity function. Further, the model predicts that insufficient numbers of microtubules protruding from the kinetochores decreases the velocity and randomizes directionality of congression movements. These predictions match changes in the chromosome behavior observed in cells with suppressed nucleation of microtubules at the kinetochore corona (RPE1 Rod{Delta}/{Delta}). In contrast, predictions of computational models based on continuous pulling forces at kinetochores differ significantly from the experimental observations. Together, live-cell observations and modeling reveal a novel mechanism that enables the efficient and synchronized arrival of chromosomes to the spindle equator. Significance StatementFor equal segregation into daughter cells, chromosomes, scattered in a large volume at the onset of cell division, must congress into a narrow plate near the equator of the mitotic spindle. Molecular mechanisms of congression remain obscure. Here we use live-cell microscopy and structural analyses to quantitatively characterize chromosome behavior during congression in human cells. From these quantifications we derive a computational model that accurately predicts directionality and velocity of chromosome movements and suggests that the force for these movements arises from stochastic, transient, minus-end directed interactions between short microtubules protruding from the kinetochores and long appropriately shaped microtubules within the spindle. The model also accurately predicts changes in chromosome behavior in cells with functionally deficient kinetochores.

cell biology↗

bioRxiv2025

Branching, crosslinking and decentralization of microtubules accelerates intracellular assembly

Before cell division, mitotic spindle is assembled from chromosomes and centrosomes. After the cell division, Golgi organelles assemble from multiple vesicles scattered across daughter cells. These are but two examples of intracellular assembly of vesicles, organelles and chromosomes made possible by dynamic microtubules. The most prominent microtubule networks are centrosome-focused asters that search for the vesicles and chromosomes, but there are also microtubules originating from the vesicles and chromosomes, raising the question whether a coordination between multiple microtubule networks optimizes the assembly process. This study uses a computational model to examine how microtubule dynamics influence the assembly of organelles from vesicles. The model includes two microtubule populations: microtubules anchored to the vesicles, which drive local clustering, and central microtubules anchored to the centrosome that aggregate the vesicles globally. Simulations show that a microtubule decentralization - balanced contribution from both microtubule populations -- accelerates the assembly of tens of vesicles, but that assigning all microtubules to hundreds of vesicles optimizes the assembly. Directionally biased microtubule growth, particularly when avoiding spontaneous catastrophe events, further accelerates the assembly. Additionally, microtubule branching, when occurring at optimal angles and spacings, enhances the assemblys efficiency. Lastly, rapid crosslinking of overlapping central and local microtubules can drastically accelerate the assembly. Applying this model to the spindle assembly in early mitosis reveals similar insights. The model suggests that the observed multiple microtubule networks optimize the intracellular assembly processes when molecular resources are limited. SIGNIFICANCEAssembly of intracellular structures is a time-sensitive process driven by multiple dynamic microtubule networks. For example, vesicles must be aggregated by microtubules to form Golgi apparatus after cell division, while mitotic spindle assembly requires bringing chromosomes closer together by microtubules growing from spindle poles and chromosomes. Delays in these processes can lead to genomic instability and disease. Using modeling, we show how microtubules originating from centrosomes, vesicles, or chromosomes can be optimally distributed to minimize the assembly time. The model reveals roles of microtubule decentralization, branching and crosslinking in accelerating assembly. The model suggests that the intracellular assembly can be optimized by diversifying microtubule networks and enhancing their interactions.

biophysics↗

bioRxiv2025

Reconstructing Noisy Gene Regulation Dynamics UsingExtrinsic-Noise-Driven Neural Stochastic Differential Equations

Proper regulation of cell signaling and gene expression is crucial for maintaining cellular function, development, and adaptation to environmental changes. Reaction dynamics in cell populations is often noisy because of (i) inherent stochasticity of intracellular biochemical reactions ("intrinsic noise") and (ii) heterogeneity of cellular states across different cells that are influenced by external factors ("extrinsic noise"). In this work, we introduce an extrinsic-noise-driven neural stochastic differential equation (END-nSDE) framework that utilizes the Wasserstein distance to accurately reconstruct SDEs from trajectory data from a heterogeneous population of cells (extrinsic noise). We demonstrate the effectiveness of our approach using both simulated and experimental data from three different systems in cell biology: (i) circadian rhythms, (ii) RPA-DNA binding dynamics, and (iii) NF{kappa}B signaling process. Our END-nSDE reconstruction method can model how cellular heterogeneity (extrinsic noise) modulates reaction dynamics in the presence of intrinsic noise. It also outperforms existing time-series analysis methods such as recurrent neural networks (RNNs) and long short-term memory networks (LSTMs). By inferring cellular heterogeneities from data, our END-nSDE reconstruction method can reproduce noisy dynamics observed in experiments. In summary, the reconstruction method we propose offers a useful surrogate modeling approach for complex biophysical processes, where high-fidelity mechanistic models may be impractical.

molecular biology↗

bioRxiv2024

Balancing limited resources in actin networks competition

In cells, multiple actin networks coexist in a dynamic manner. These networks compete for a common pool of actin monomers and actin-binding proteins. Interestingly, this competition does not result in the mere survival of the more consuming networks. Moreover, the co-existence of networks with various strengths is key to cell adaption to external changes. However, a comprehensive view of how these networks coexist in this competitive environment, where resources are limited, is still lacking. To address this question, we used a reconstituted system, in closed microwells, consisting of beads propelled by actin polymerization or micropatterns functionalized with lipids capable of initiating polymerization close to a membrane. This system enabled us to build dynamic actin architectures, competing for a limited pool of proteins, over a period of hours. We demonstrated the importance of protein turnover for the coexistence of actin networks, showing it ensures resource distribution between weak and strong networks. However, when competition becomes too intense, turnover alone is insufficient, leading to a selection process that favors the strongest networks. Consequently, we emphasize the importance of competition strength, which is defined by the turnover rate, the amount of available protein, and the number of competing structures. More generally, this work illustrates how turnover allows biological populations with various competition strengths to coexist despite resource constraints. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=97 SRC="FIGDIR/small/612098v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@370343org.highwire.dtl.DTLVardef@1b75a2forg.highwire.dtl.DTLVardef@81e55dorg.highwire.dtl.DTLVardef@1f97452_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical AbstractC_FLOATNO C_FIG

cell biology↗

bioRxiv2024

Galvanotactic directionality of cell groups depends on group size

Motile cells migrate directionally in the electric field in a process known as galvanotaxis, important and under-investigated phenomenon in wound healing and development. We previously reported that individual fish keratocyte cells migrate to the cathode in electric fields, that inhibition of PI3 kinase reverses single cells to the anode, and that large cohesive groups of either unperturbed or PI3K-inhibited cells migrate to the cathode. Here we find that small uninhibited cell groups move to the cathode, while small groups of PI3K-inhibited cells move to the anode. Small groups move faster than large groups, and groups of unperturbed cells move faster than PI3K-inhibited cell groups of comparable sizes. Shapes and sizes of large groups change little when they start migrating, while size and shapes of small groups change significantly, lamellipodia disappear from the rear edges of these groups, and their shapes start to resemble giant single cells. Our results are consistent with the computational model, according to which cells inside and at the edge of the groups pool their propulsive forces to move but interpret directional signals differently. Namely, cells in the group interior are directed to the cathode independently of their chemical state. Meanwhile, the edge cells behave like individual cells: they are directed to the cathode/anode in uninhibited/PI3K-inhibited groups, respectively. As a result, all cells drive uninhibited groups to the cathode, while larger PI3K-inhibited groups are directed by cell majority in the group interior to the cathode, while majority of the edge cells in small groups win the tug-of-war driving these groups to the anode. Significance statementMotile cells migrate directionally in electric fields. This behavior - galvanotaxis - is important in many physiological phenomena. Individual fish keratocytes migrate to the cathode, while inhibition of PI3K reverses single cells to the anode. Uninhibited cell groups move to the cathode. Surprisingly, groups of PI3K-inhibited cells exhibit bidirectional behavior: larger/smaller groups move to the cathode/anode, respectively. A mechanical model suggests that inner and outer cells interpret directional signals differently, and that a tug-of-war between the outer and inner cells directs the cell groups. These results shed light on general principles of collective cell migration.

cell biology↗

bioRxiv2023

Helical motors and formins synergize to compact chiral filopodial bundles: a theoretical perspective.

Chiral actin bundles have been shown to play an important role in cell dynamics, but our understanding of the molecular mechanisms which combine to generate chirality remains incomplete. We numerically simulate a crosslinked filopodial bundle under the actions of helical myosin motors and/or formins and examine the collective buckling and twisting of the actin bundle. We find that the myosin spinning action effectively "braids" the bundle, compacting it, generating buckling, and enhancing crosslinking. Stochastic fluctuations of actin polymerization rates also contribute to filament buckling and bending of the bundle. Faster turnover of transient crosslinks attenuates the buckling and enhances coiling and compaction of the bundle. Formin twisting action by itself is not effective in inducing filopodial coiling and compaction, but co-rotating formins synergize with helical motors to coil and compact the actin bundle. We discuss implications of our findings for mechanisms of cytoskeletal chirality.

cell biology↗

bioRxiv2023

Focal adhesions are controlled by microtubules through local contractility regulation

Microtubules regulate cell polarity and migration by local activation of focal adhesion turnover, but the mechanism of this process is insufficiently understood. Molecular complexes containing KANK family proteins connect microtubules with the major component of focal adhesions, talin. Local optogenetic activation of KANK1-mediated links which promoted microtubule targeting to individual focal adhesion resulting in its centripetal sliding and rapid disassembly. The sliding is preceded by a local increase of traction force due to accumulation of myosin-II and actin in the proximity of the focal adhesion. Knockdown of Rho activator GEF-H1 prevented development of traction force and abolished sliding and disassembly of focal adhesion upon KANK activation. Other players participating in microtubule-driven KANK-dependent focal adhesion disassembly include kinases ROCK and PAK, as well as microtubules/focal adhesions associated proteins Kinesin-1, APC and TAT. Finally, we propose a physical model of a microtubule-driven focal adhesion disruption involving local GEF-H1/RhoA/ROCK dependent activation of contractility which is consistent with experimental data.

cell biology↗

bioRxiv2022

Friction patterns guide actin network contraction

The shape of cells is the outcome of the balance of inner forces produced by the actomyosin network and the resistive forces produced by cell adhesion to their environment. The specific contributions of contractile, anchoring and friction forces to network deformation rate and orientation are difficult to disentangle in living cells where they influence each other. Here, we reconstituted contractile acto-myosin networks in vitro to study specifically the role of the friction forces between the network and its anchoring substrate. To modulate the magnitude and spatial distribution of friction forces, we micropatterned actin nucleation promoting factors on glass or on a lipid bilayer. We adapted their concentrations on each surface to induce the assembly of actin networks of similar densities, and compare the deformation of the network toward the centroid of the pattern shape upon myosin-induced contraction. We found that actin network deformation was faster and more coordinated on lipid bilayers than on glass, showing the resistance of friction to network contraction. To further study the role of the spatial distribution of these friction forces, we designed heterogeneous micropatterns made of glass and lipids. The deformation upon contraction was no longer symmetric but biased toward the region of higher friction. Furthermore, we showed that the pattern of friction could robustly drive network contraction and dominate the contribution of asymmetric distributions of myosins. Therefore, we demonstrate that during contraction both the active and resistive forces are essential to direct the actin network deformation. Significance statementCell shape changes are controlled by complex sets of mechanical forces of various origins. Numerous studies have been dedicated to the role of active forces, originating from molecular motors and filament polymerization, but much less is known about the guiding role of resistive forces. Here we show that a non-uniform distribution of friction forces between a contracting acto-myosin network and its underlying substrate can direct its deformation as it contracts. Our results suggest that the contribution of resistive forces, such as anchoring forces but also less specific viscous forces along cell surface, can be as significant as those of active forces in driving network deformation and should be considered in mechanical models describing the regulation of cell shape and movements.

biophysics↗

bioRxiv2022

Recycling limits the lifetime of actin turnover

Intracellular organization is largely mediated by the actin turnover. Cellular actin networks consume matter and energy to sustain their dynamics, while maintaining their appearance. This behavior, called dynamic steady state, enables cells to sense and adapt to their environment. However, how structural stability can be maintained during the constant turnover of a limited actin monomer pool is poorly understood. To answer this question, we developed an experimental system using actin bead motility in a compartment with a limited amount of monomer. We used the speed and the size of the actin comet tails to evaluate the systems monomer consumption and its lifetime. We established the relative contribution of actin assembly, disassembly and recycling for a bead movement over tens of hours. Recycling mediated by cyclase-associated proteins is the key step in allowing the reuse of monomers for multiple assembly cycles. Energy supply and protein aging are also factors that limit the lifetime of actin turnover. This work reveals the balancing mechanism for long-term network assembly with a limited amount of building blocks.

cell biology↗

bioRxiv2022

Size-dependent transition from steady contraction to waves in actomyosin networks with turnover

Actomyosin networks play essential roles in many cellular processes including intracellular transport, cell division, and cell motility, exhibiting a myriad of spatiotemporal patterns. Despite extensive research, how the interplay between network mechanics, turnover and geometry leads to these different patterns is not well understood. We focus on the size-dependent behavior of contracting actomyosin networks in the presence of turnover, using a reconstituted system based on cell extracts encapsulated in water-in-oil droplets. We find that the system can self-organize into different global contraction patterns, exhibiting persistent contractile flows in smaller droplets and periodic contractions in the form of waves or spirals in larger droplets. The transition between continuous and periodic contraction occurs at a characteristic length scale that is inversely dependent on the network contraction rate. These dynamics are recapitulated by a theoretical model, which considers the coexistence of different local density-dependent mechanical states with distinct rheological properties. The model shows how large-scale contractile behaviors emerge from the interplay between network percolation essential for long-range force transmission and rearrangements due to advection and turnover. Our findings thus demonstrate how varied contraction patterns can arise from the same microscopic constituents, without invoking specific biochemical regulation, merely by changing the systems geometry.

biophysics↗

bioRxiv2021

Mechanical torque promotes bipolarity of the mitotic spindle through multi-centrosomal clustering

Intracellular forces shape cellular organization and function. One example is the mi-totic spindle, a cellular machine consisting of multiple chromosomes and centrosomes which interact via dynamic microtubule filaments and motor proteins, resulting in complicated spatially dependent forces. For a cell to divide properly, is important for the spindle to be bipolar, with chromosomes at the center and multiple centrosomes clustered into two poles at opposite sides of the chromosomes. Experimental observations show that in unhealthy cells, the spindle can take on a variety of patterns. What forces drive each of these patterns? It is known that attraction between centrosomes is key to bipolarity, but what the prevents the centrosomes from collapsing into a monopolar configuration? Here, we explore the hypothesis that torque rotating chromosome arms into orientations perpendicular to the centrosome-centromere vector promotes spindle bipolarity. To test this hypothesis, we construct a pairwise-interaction model of the spindle. On a continuum version of the model, an integro-PDE system, we perform linear stability analysis and construct numerical solutions which display a variety of spatial patterns. We also simulate a discrete particle model resulting in a phase diagram that confirms that the spindle bipolarity emerges most robustly with torque. Altogether, our results suggest that rotational forces may play an important role in dictating spindle patterning.

biophysics↗

bioRxiv2021

F-actin bending facilitates net actomyosin contraction by inhibiting expansion with plus-end-located myosin motors

Contraction of actomyosin networks underpins important cellular processes including motility and division. The mechanical origin of actomyosin contraction is not fully-understood. We investigate whether contraction arises on the scale of individual filaments, without needing to invoke network-scale interactions. We derive discrete force-balance and continuum partial differential equations for two symmetric, semi-flexible actin filaments with an attached myosin motor. Assuming the system exists within a homogeneous background material, our method enables computation of the stress tensor, providing a measure of contractility. After deriving the model, we use a combination of asymptotic analysis and numerical solutions to show how F-actin bending facilitates contraction on the scale of two filaments. Rigid filaments exhibit polarity-reversal symmetry as the motor travels from the minus to plus-ends, such that contractile and expansive components cancel. Filament bending induces a geometric asymmetry that brings the filaments closer to parallel as a myosin motor approaches their plus-ends, decreasing the effective spring force opposing motor motion. The reduced spring force enables the motor to move faster close to filament plus-ends, which reduces expansive stress and gives rise to net contraction. Bending-induced geometric asymmetry provides both new understanding of actomyosin contraction mechanics, and a hypothesis that can be tested in experiments.

biophysics↗

bioRxiv2021

Interplay between Brownian motion and cross-linking kinetics controls bundling dynamics in actin networks

Morphology changes in cross-linked actin networks are important in cell motility, division, and cargo transport. Here we study the transition from a weakly cross-linked network of actin filaments to a heavily cross-linked network of actin bundles through microscopic Brownian dynamics simulations. We show that this transition occurs in two stages: first, a composite bundle network of small and highly aligned bundles evolves from cross linking of individual filaments; second, small bundles coalesce into the clustered bundle state. We demonstrate that Brownian motion speeds up the first stage of this process at a faster rate than the second. We quantify the time to reach the composite bundle state and show that it is a strong function of mesh size only when the concentration of cross links is small, and that it remains roughly constant if we decrease the relative ratio of cross linkers as we increase the actin concentration. Finally, we examine the dependence of the bundling timescale on filament length, finding that shorter filaments bundle faster because they diffuse faster.

cell biology↗