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Biology subjects

Han, S. J.

Publications and source records attributed to Han, S. J..

At least 19 recordsLinked to original sources

Cornealia: automated collective order analysis reveals density-dependent reorganization of donor corneal endothelium

The corneal endothelium is a non-regenerative monolayer whose health determines transplant success, yet donor tissue is assessed only by single-cell metrics that ignore how the monolayer is organized collectively. A physics-based spring constant K, derived from the radial distribution function of cell positions, captures this collective order but has remained limited to semi-manual studies without physical interpretation. Here we present Cornealia, an automated pipeline for collective-order and intercellular-force analysis. In cultured endothelial cells, collective order declines with passaging and is higher under growth-factor conditions that preserve N-cadherin junctions, differences invisible to cell density and hexagonality. Across 2,177 donor cornea images from two cohorts, collective order, distinct from classical metrics, responds most to mechanical perturbation: corneas with endothelial cell density above 2,400 cells/mm^2 mostly gain order, whereas less dense ones lose it, on one curve shared by both cohorts. Reconstructed intercellular forces track these changes. This switch lies within the minimum donor densities used by eye banks, suggesting a mechanical basis for these clinical thresholds and establishing collective order as an automatable measure of endothelial quality.

bioinformatics↗

Signal Associa: hot tumors elicit field-spanning NK cell coordination linked to their recruitment

Cells coordinate through coupled dynamics, yet whether observed correlations reflect genuine coupling is rarely tested. Signal Associa is an open-source framework uniting six coupling methods with automated stationarization and surrogate testing. Benchmarking against six ground truth systems reveals a trichotomy of coupling regimes, each with a different best method: correlation for coupling carried by shared trends and cycles, Granger causality for linear stochastic coupling, and convergent cross-mapping for nonlinear coupling; agreement across methods identifies the regime from data. In 13 movies of natural killer (NK) cells across three colorectal tumor microenvironments, NK cells formed field-spanning coupling networks at a conserved rate; at matched exposure to tumor signal, NK cells around hot tumors were more globally integrated, and hot tumors with a more integrated NK network tended to attract more NK cells. In focal adhesions, stiffness strengthened vinculin-FAK coupling, most at protruding edges. Surrogates cut lagged-correlation false positives from 23-92% to about 5%.

systems biology↗

Collagen V Presented at the Cell-Substrate Interface Mimics Substrate Stiffening to Enhance Fibroblast Traction, Adhesion Turnover, and Persistent Migration

Collagen type V (Col-V) is a minor fibrillar collagen that regulates collagen fibril assembly, and its haploinsufficiency causes classical Ehlers-Danlos syndrome, in which wound healing is delayed. Whether Col-V also changes how fibroblasts adhere to, pull on, and migrate across a collagen-presenting surface has not been tested directly. Here, we covalently coupled Col-I or Col-V to soft (2.7 kPa) silicone substrates and quantified the mechanical response of NIH/3T3 fibroblasts. On Col-V, cells generated about 1.5-fold higher traction, spread more, and formed smaller focal adhesions that each carried more force. Adhesions on Col-V assembled and disassembled faster. Single fibroblasts on Col-V migrated more slowly but more persistently, and fibroblast monolayers closed a 500 micrometer gap faster. Raising substrate stiffness to 13 kPa reproduced this phenotype on Col-I, including higher traction, larger spread area, and smaller focal adhesions, indicating that Col-V presentation produces an adhesion state that otherwise requires a stiffer substrate. In separate reconstituted collagen hydrogels, co-assembly with 10 to 20% Col-V yielded thinner, straighter fibrils, and 20% Col-V increased the indentation modulus of the gel. These results identify the collagen type presented at the cell-material interface as a design parameter that can partly substitute for bulk stiffness in controlling fibroblast traction and migration, and they suggest Col-V as a tunable component of collagen-based biomaterials.

bioengineering↗

Regulated RIAM-Talin Engagement Controls Adhesion Stability and Mechanical Output

RIAM (Rap1-GTP-interacting adaptor molecule) links Rap1 to talin-1 to promote integrin activation and is normally enriched at nascent adhesions. How the duration of RIAM-talin engagement influences adhesion dynamics and force transmission remains unclear. Here, we used a RIAM chimera in which the native talin-binding site was replaced with the talin-binding motif of Kank2 to enforce sustained talin association and redistribute RIAM modules to mature adhesions. This talin-tethered RIAM chimera enhanced integrin activation, accelerated both adhesion assembly and disassembly, reduced adhesion lifetime, increased the fraction of nascent adhesions nucleated by RIAM, and elevated cellular traction forces. Notably, while integrin activation by the chimera was largely Rap1-independent, Rap1 binding remained necessary for optimal adhesion turnover kinetics and full traction force generation. These findings demonstrate that prolonged talin engagement of RIAM is sufficient to reprogram adhesion dynamics and reveal a separable role for Rap1 in coordinating force transmission downstream of integrin activation. Together, our results highlight the importance of regulating the residence and engagement mode of RIAM at talin for controlling adhesion plasticity and mechanotransduction.

cell biology↗

ERK builds a population of short-lived nascent adhesions that produce persistent edge protrusion and cell migration

Cell migration is realized through the fast and persistent protrusion of a leading edge in the direction of movement. The actin and adhesion structures that build edge protrusions are integrated such that pro-migration signaling pathways must control both assemblies to induce protrusion. Understanding the contribution of adhesion regulation has been complicated by the inability to selectively assay the nascent adhesions that promote edge protrusion. Here, we dissect how the core RAS[->]RAF[->]MEK[->]ERK pathways control of nascent adhesions contributes to edge protrusion and cell migration by targeting an ERK FRET biosensor to adhesions and quantifying ERKs spatial and temporal activity. We find that ERK is activated in the assembling, membrane-proximal region of nascent adhesions through adhesion scaffold paxillin, which interacts with the ERK activator MEK. Tracking nascent adhesion dynamics during cell migration showed that ERK promotes both nascent adhesion assembly and disassembly to create a population of nascent adhesions with short lifetimes. MEK inhibition is partially complemented by expression of a talin R8vvv mutant that increases the nascent adhesion population, demonstrating the significance of ERKs adhesion regulation for edge protrusion and migration persistence. These findings suggest that when new adhesions initiate, the ERK activation level dictates adhesion assembly and disassembly rates to specifically build nascent adhesions that rapidly turnover, an adhesion population that promotes protrusion persistence and migration. SignificanceCell migration is essential for development, healing, and cancer spread. To move, cells need to build and break tiny structures called nascent adhesions, specifically at their edge that protrudes in the direction of movement. We discovered that ERK, a key signaling protein activated during development and cancer, helps create a fast-turning-over population of these adhesions, which supports steady movement. Using new biosensors and adhesion tracking, we showed ERK is active in the assembling part of the adhesion, where it promotes both assembly and disassembly. Increasing the nascent adhesion population helps cells move when ERK is blocked. This work reveals how ERK controls cell movement by balancing adhesion dynamics and introduces tools to study similar processes in other signaling pathways.

cell biology↗

CNS-penetrant NLRP3 inhibitor achieves durable weight loss and reverses hypothalamic inflammation in diet-induced obesity

The NLRP3 inflammasome is a key mediator of innate immunity that integrates inflammatory and metabolic stress signals. Increased and/or chronic activation of this critical pathway has been implicated in obesity, with hypothalamic neuroinflammation linked to dysregulation of energy balance. TN-783 is an investigational, CNS-penetrant, small-molecule NLRP3 inhibitor that potently suppressed inflammasome activation across multiple in vitro assays. In diet-induced obese (DIO) mice, only TN-783, and not the peripherally restricted NLRP3 inhibitor TN-101, produced progressive and sustained weight loss, underscoring the requirement for central target engagement. Weight loss was driven by a persistent reduction in food intake across both acute and chronic phases, without altering energy expenditure. This effect was further characterized by selective reduction of fat mass, with minimal impact on lean tissues. Mechanistically, NLRP3 inhibition attenuated DIO-induced hypothalamic neuroinflammation and partially reversed obesity-associated molecular changes based on transcriptomic and proteomic profiling of the hypothalamus. Beyond monotherapy, TN-783 enhanced the effects of the GLP-1 receptor agonist semaglutide by amplifying weight loss, reinitiating weight loss after semaglutide effect had plateaued, and maintaining the weight loss benefit after semaglutide withdrawal. Discontinuation of TN-783 resulted in reversal of both weight and feeding effects, indicating that its therapeutic activity requires ongoing target engagement rather than permanent remodeling of metabolic pathways. Collectively, these observations support central NLRP3 inhibition as a distinct and promising approach for obesity treatment, offering robust induction and sustained maintenance of weight loss while preserving reversibility.

neuroscience↗

Mapping the evolution of computationally designed protein binders

Computational protein design enables the generation of binders that target specific epitopes on proteins. However, current approaches often require substantial screening from which hits require further affinity maturation. Methods for experimentally improving designed proteins and exploring their sequence-affinity landscapes could therefore streamline the development of high-affinity binders and inform future design strategies. Here, we use OrthoRep, a system for continuous hypermutation in vivo, to drive the evolution of computationally designed mini protein binders ("minibinders") that target a mammalian receptor. Despite their small sizes (59-72 amino acids), we successfully affinity matured multiple minibinders through strong selection for improved binding and also sampled new regions of minibinder fitness landscapes through extensive neutral drift. One evolved minibinder variant was used to construct a combinatorially complete sequence-affinity map for its six affinity increasing mutations, which revealed nearly full additivity in their contributions to binding. Another minibinder was subjected to both deep mutational scanning and extensive evolution under weak selection, resulting in an evolutionarily diverged collection of binder sequences that revealed non-additive relationships among mutations. Our results highlight that the affinity of computationally designed binders can be rapidly increased through evolution and provide a scalable approach for the evolutionary exploration and subsequent mapping of sequence-affinity landscapes. We suggest that this work will complement protein binder design both as a reliable experimental optimization process and as a vehicle for generating new training data.

synthetic biology↗

Kinetic Modeling of mant-ATP Turnover to Interpret the Biochemically Defined Myosin Super-Relaxed State

The fluorescent ATP analog mant-ATP has become a valuable tool for quantifying occupancy of the myosin super-relaxed (SRX) state, a biochemically inactive state of myosin in striated muscle. Interpretation of mant-ATP fluorescence decay kinetics is confounded by inconsistencies in state definitions and kinetic assumptions. Here, we develop a mass-action kinetic model of myosin cross-bridge cycling and mant-ATP turnover to reconcile these discrepancies and provide a mechanistic framework for interpreting SRX measurements. Our model simulates ATP label-chase experiments and demonstrates that conventional double-exponential fitting methods do not directly quantify SRX occupancy. Instead, we show that slow and fast decay phases of mant-ATP fluorescence arise from label redistribution among kinetically distinct states, not state populations in equilibrium. The model resolves several apparent paradoxes identified in recent studies by reproducing experimental observations without requiring SRX and DRX kinetic isolation or implausible equilibrium constants. Simulations further quantify the impact of experimental factors--such as ADP accumulation, photobleaching, and initial rigor state occupancy--on fluorescence kinetics and SRX estimates. These results support a revised framework for SRX quantification and suggest that label-chase experiments must be interpreted using mechanistic models to accurately assess myosin state distributions and transition kinetics. SIGNIFICANCEThe relative occupancy of myosin in the super-relaxed state (SRX) is a key determinant of basal ATP turnover in muscle. Measurement of ATP exchange using the fluorescent analog mant-ATP is used to assess the relative population of myosin in the SRX versus the disordered relaxed (DRX) state. Existing approaches to analyzing data from these experiments use double exponential fits to represent the mant-ATP decay in the chase-phase of the experiment. However, quantitative and mechanistic interpretations based on these analyses remain ambiguous. We present a mechanistic model of myosin ATP turnover that reproduces observed fluorescence decays under defined conditions. The results indicate that conventional interpretations, while qualitatively reasonable, are quantitatively inconsistent, as the observed slow and fast phases are predicted to arise from ligand redistribution rather than distinct equilibrium states. This framework enables rigorous, model-based interpretation of mant-ATP assays to help clarify how myosin kinetics are reflected in mant-ATP loading-chase experiments and experimental conditions may influence apparent SRX kinetics.

biophysics↗

PKP2 orchestrates OXPHOS expression in cardiomyocytes via a PGC1α-dependent mechanism

Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disease where the majority of ACM patients carry a (likely) pathogenic variant in desmosomal genes, predominantly in plakophilin-2 (PKP2). While the genetic cause of the disease is well studied, the molecular disease-driving mechanisms and how exercise can drive disease progression remain poorly understood. In this study, we identified the oxidative phosphorylation (OXPHOS) pathway to be downregulated in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and human explanted hearts carrying pathogenic PKP2 variants. The reduced expression of OXPHOS related genes was a result of lower PPARGC1A expression which led to decreased mitochondrial spare capacity in PKP2 mutant hiPSC-CMs. Induction of PPARGC1A expression partially restored the expression of OXPHOS components and improved contractility in PKP2 mutant cells. These results suggest that improving oxidative capacity through modulation of PPARGC1A in cardiomyocytes could be considered as a new therapeutic target for ACM patients in the future.

molecular biology↗

TRPV4 Dominates High Shear-Induced Initial Traction Response and Long-Term Relaxation Over Piezo1

Modulation of endothelial traction is critical for the responses of endothelial cells to fluid shear stress (FSS), which has profound implications for vascular health and atherosclerosis. Previously, we demonstrated that under high FSS, endothelial cells rapidly increase traction forces, followed by relaxation, with traction aligning in the flow direction. In contrast, low shear preconditioning induces a modest short-term increase in traction (<30 min), followed by a secondary long-term (>14 hr) rise, with traction/cells aligning perpendicular to the flow. The upstream mechanosensors driving these responses, however, remain unknown. Here, we sought the roles of Piezo1 and TRPV4 ion channels in shear-induced traction modulation. We report that HUVECs with Piezo1 silencing reduced the initial traction rise in half under high FSS compared to those by WT cells, while not affecting the traction modulation in response to low FSS or traction/cell alignment to the flow direction. Conversely, cells with siTRPV4 fully abrogated the initial traction rise, as well as alignment of traction and cells, in response to both high and low FSS conditions. Dual inhibition of Piezo1 and TRPV4 further impaired both initial and long-term traction under high FSS. Interestingly, dual-inhibited cells displayed larger initial traction responses to low FSS compared to control cells, suggesting the involvement of alternative calcium-independent pathways that become dominant when both ion channels are nonfunctional. Additionally, either ion channel inhibition led to secondary long-term traction increase even under high FSS condition. These findings suggest that while both Piezo1 and TRPV4 channels contribute to shear mechanotransduction, TRPV4 plays more dominant role than Piezo1 in mediating the initial traction rise and sustaining long-term relaxation under high or low shear stress, highlighting their critical and distinct contributions to endothelial mechanotransduction and remodeling.

cell biology↗

Differential cell-ECM interaction of rhabdomyosarcoma subtypes regulated by PAX3-FOXO1

Rhabdomyosarcoma (RMS) is the most common childhood soft tissue sarcoma, with two subtypes: Fusion-positive RMS (FPRMS), which has the PAX3-FOXO1 fusion gene, and fusion-negative RMS (FNRMS). Despite their distinct characteristics, treatments mainly rely on conventional chemotherapies without considering these differences. This study highlights that FNRMS cells exhibit significantly heightened interaction with the extracellular matrix (ECM) compared to FPRMS cells. Using single-cell RNA sequencing of skeletal muscle tissues and RNA sequencing of RMS samples, we identified the upregulation of genes related to cell-ECM interaction and TGF{beta} signaling in FNRMS compared to FPRMS. We also confirmed enhanced cell-ECM interaction stimulated by TGF{beta} signaling in FNRMS cells, using confocal reflection microscopy to monitor dynamic cell-ECM interaction and a live-cell sensor to quantitatively assess TGF{beta} signaling activity. Additionally, we discovered that the PAX3-FOXO1 fusion gene, characteristic of FPRMS, stimulated nitric oxide synthesis, which suppresses TGF{beta} signaling and reduces cell-ECM interaction. These findings suggest that PAX3-FOXO1 determines the diminished cell-ECM interactions in FPRMS. Experimental data show higher sensitivity of FNRMS to cell-ECM interaction disruption and TGF{beta} inhibition. Furthermore, the diminished cell-ECM interaction in FPRMS, allowing cells to survive in the ectopic environment through circulation, may partly explain its higher metastatic potential compared to FNRMS.

cell biology↗

N-Myc and STAT Interactor is an endometriosis suppressor.

In patients with endometriosis, refluxed endometrial fragments evade host immunosurveillance, developing into endometriotic lesions. However, the mechanisms underlying this evasion have not been fully elucidated. N-Myc and STAT Interactor (NMI) have been identified as key players in host immunosurveillance, including interferon (IFN)-induced cell death signaling pathways. NMI levels are markedly reduced in the stromal cells of human endometriotic lesions due to modulation by the Estrogen Receptor beta/Histone Deacetylase 8 axis. Knocking down NMI in immortalized human endometrial stromal cells (IHESCs) led to elevated RNA levels of genes involved in cell-to-cell adhesion and extracellular matrix signaling following IFNA treatment. Furthermore, NMI knockdown inhibited IFN-regulated canonical signaling pathways, such as apoptosis mediated by Interferon Stimulated Gene Factor 3, and necroptosis upon IFNA treatment. In contrast, NMI knockdown with IFNA treatment activated non-canonical IFN-regulated signaling pathways that promote proliferation, including {beta}-Catenin and AKT signaling. Moreover, NMI knockdown in IHESCs stimulated ectopic lesions growth in mouse endometriosis models. Therefore, NMI is a novel endometriosis suppressor, enhancing apoptosis and inhibiting proliferation and cell adhesion of endometrial cells upon IFN exposure.

molecular biology↗

Modular Phoneme Processing in Human Superior Temporal Gyrus

Modular organization is fundamental to cortical processing, but its presence is human association cortex is unknown. We characterized phoneme processing with 128-1024 channel micro-arrays at 50-200m pitch on superior temporal gyrus of 7 patients. High gamma responses were highly correlated within [~]1.7mm diameter modules, sharply delineated from adjacent modules with distinct time-courses and phoneme-selectivity. We suggest that receptive language cortex may be organized in discrete processing modules.

neuroscience↗

Impact of Low Shear Stress Preconditioning on Endothelial Cell Traction and Alignment in Response to High Shear Stress

Within the vascular system, endothelial cells (ECs) are exposed to fluid shear stress (FSS), a mechanical force exerted by blood flow that is critical for regulating cellular tension and maintaining vascular homeostasis. The way ECs react to FSS varies significantly; while high, laminar FSS supports vasodilation and suppresses inflammation, low or disturbed FSS can lead to endothelial dysfunction and increase the risk of cardiovascular diseases. Yet, the adaptation of ECs to dynamically varying FSS remains poorly understood. This study focuses on the dynamic responses of ECs to brief periods of low FSS, examining its impact on endothelial traction--a measure of cellular tension that plays a crucial role in how endothelial cells respond to mechanical stimuli. By integrating traction force microscopy (TFM) with a custom-built flow chamber, we analyzed how human umbilical vein endothelial cells (HUVECs) adjust their traction in response to shifts from low to high shear stress. We discovered that initial exposure to low FSS prompts a marked increase in traction force, which continues to rise over 10 hours before slowly decreasing. In contrast, immediate exposure to high FSS causes a quick spike in traction followed by a swift reduction, revealing distinct patterns of traction behavior under different shear conditions. Importantly, the direction of traction forces and the resulting cellular alignment under these conditions indicate that the initial shear experience dictates long-term endothelial behavior. Our findings shed light on the critical influence of short-lived low-shear stress experiences in shaping endothelial function, indicating that early exposure to low FSS results in enduring changes in endothelial contractility and alignment, with significant consequences for vascular health and the development of cardiovascular diseases.

cell biology↗

Steroid Receptor Coactivator-3 is a Key Modulator of Regulatory T Cell-Mediated Tumor Evasion

AbstractsSteroid receptor coactivator 3 (SRC-3) is most strongly expressed in regulatory T cells (Tregs) and B cells, suggesting that it plays an important role in the regulation of Treg function. Using an aggressive E0771 mouse breast cell line syngeneic immune-intact murine model, we observed that breast tumors were permanently eradicated in a genetically engineered tamoxifen-inducible Treg-cell specific SRC-3 knockout (KO) female mouse that does not possess a systemic autoimmune pathological phenotype. A similar eradication of tumor was noted in a syngeneic model of prostate cancer. A subsequent injection of additional E0771 cancer cells into these mice showed continued resistance to tumor development without the need for tamoxifen induction to produce additional SRC-3 KO Tregs. SRC-3 KO Tregs were highly proliferative and preferentially infiltrated into breast tumors by activating the Chemokine (C-C motif) ligand (Ccl) 19/Ccl21/ Chemokine (C-C motif) Receptor (Ccr)7 signaling axis, generating antitumor immunity by enhancing the interferon-{gamma}/C-X-C Motif Chemokine Ligand (Cxcl) 9 signaling axis to facilitate the entrance and function of effector T cells and Natural Killer cells. SRC-3 KO Tregs also show a dominant effect by blocking the immune suppressive function of WT Tregs. Importantly, a single adoptive transfer of SRC-3 KO Tregs into wild-type E0771 tumor-bearing mice can completely abolish pre-established breast tumors by generating potent antitumor immunity with a durable effect that prevents tumor reoccurrence. Therefore, treatment with SRC-3 deleted Tregs represents a novel approach to completely block tumor growth and recurrence without the autoimmune side-effects that typically accompany immune checkpoint modulators. Significance statementTregs are essential in restraining immune responses for immune homeostasis. SRC-3 is a pleiotropic coactivator, the second-most highly expressed transcriptional coactivator in Tregs, and a suspect in Treg function. The disruption of SRC-3 expression in Tregs leads to a complete lifetime eradication of tumors in aggressive syngeneic breast cancer mouse models because deletion of SRC-3 alters the expression of a wide range of key genes involved in efferent and afferent Treg signaling. SRC-3KO Tregs confer this long-lasting protection against cancer recurrence in mice without an apparent systemic autoimmune pathological phenotype. Therefore, treatment with SRC-3 deleted Tregs could represent a novel and efficient future target for eliminating tumor growth and recurrence without the autoimmune side-effects that typically accompany immune checkpoint modulators.

cancer biology↗

Nascent adhesions differentially regulate lamellipodium velocity and persistence

Cell migration is essential to physiological and pathological biology. Migration is driven by the motion of a leading edge, in which actin polymerization pushes against the edge and adhesions transmit traction to the substrate while membrane tension increases. How the actin and adhesions synergistically control edge protrusion remains elusive. We addressed this question by developing a computational model in which the Brownian ratchet mechanism governs actin filament polymerization against the membrane and the molecular clutch mechanism governs adhesion to the substrate (BR-MC model). Our model predicted that actin polymerization is the most significant driver of protrusion, as actin had a greater effect on protrusion than adhesion assembly. Increasing the lifetime of nascent adhesions also enhanced velocity, but decreased the protrusions motional persistence, because filaments maintained against the cell edge ceased polymerizing as membrane tension increased. We confirmed the model predictions with measurement of adhesion lifetime and edge motion in migrating cells. Adhesions with longer lifetime were associated with faster protrusion velocity and shorter persistence. Experimentally increasing adhesion lifetime increased velocity but decreased persistence. We propose a mechanism for actin polymerization-driven, adhesion-dependent protrusion in which balanced nascent adhesion assembly and lifetime generates protrusions with the power and persistence to drive migration.

cell biology↗

Black Dots: Microcontact-Printed, Reference-Free Traction Force Microscopy

Measuring the traction forces produced by cells provides insight into their behavior and physiological function. Here, we developed a technique (dubbed black dots) that microcontact prints a fluorescent micropattern onto a flexible substrate to measure cellular traction forces without constraining cell shape or needing to detach the cells. To demonstrate our technique, we assessed human platelets, which can generate a large range of forces within a population. We find platelets that exert more force have more spread area, are more circular, and have more uniformly distributed F-actin filaments. As a result of the high yield of data obtainable by this technique, we were able to evaluate multivariate mixed effects models with interaction terms and conduct a clustering analysis to identify clusters within our data. These statistical techniques demonstrated a complex relationship between spread area, circularity, F-actin dispersion, and platelet force, including cooperative effects that significantly associate with platelet traction forces. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=79 SRC="FIGDIR/small/454500v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1da5eeeorg.highwire.dtl.DTLVardef@18e939aorg.highwire.dtl.DTLVardef@17c7198org.highwire.dtl.DTLVardef@105c97c_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Direct Arp2/3-vinculin binding is essential for cell spreading, but only on compliant substrates and in 3D

Cells modify their shape in response to the extracellular environment through dynamic remodeling of the actin cytoskeleton by actin-binding proteins (ABPs) 1-4. The relation between actin dynamics and spreading is well-understood for cells on flat glass coverslips; much less is known about cell morphogenesis in compliant three-dimensional environments, and, in particular, how ABPs contribute to this process 5. Here, we knocked-out a diverse set of ABPs, and evaluated the effect of each on cell spreading on planar glass surfaces (2D) and in reconstituted collagen gels (3D). Our morphometric analyses identify the Arp2/3 complex and its associated regulatory genes among the ABPs that contribute most strongly to cell spreading in 3D, but marginally in 2D. Cells lacking Arp3 have reduced spreading specifically in 3D, and display stiffness-dependent cell-matrix adhesion defects. Through manipulation of vinculin activity, we determine that the Arp3 knock-out phenotype largely arises from the lack of direct interaction between vinculin and Arp2/3 complex. This interaction is dispensable for cell spreading in 2D. These data highlight that actin architectural features necessary for adhesion formation and cell spreading in 3D are efficiently compensated on flat and stiff surfaces.

cell biology↗