Mastodawn

📰 "Formation of the moving junction is the nexus for host cytoskeletal remodelling during Plasmodium falciparum invasion of human erythrocytes"
https://www.biorxiv.org/content/10.64898/2026.03.29.715162v1?rss=1
#Actomyosin

Formation of the moving junction is the nexus for host cytoskeletal remodelling during Plasmodium falciparum invasion of human erythrocytes

Plasmodium falciparum invasion of human erythrocytes is a complex and tightly coordinated process, involving host cell attachment, moving junction formation and engagement of the parasites actomyosin motor. The temporal precision of these events is mediated by distinct ligand-receptor interactions and the sequential release of the merozoites apical organelles. What remains unclear is how these molecular and biophysical interactions enable Plasmodium to bypass the stable erythrocyte membrane-cytoskeletal complex. Here, several P. falciparum lines expressing different fluorescently tagged apical organelle proteins, were imaged with lattice light sheet microscopy (LLSM) to determine the timing of cytoskeletal disassembly and apical organelle release. Blocking the AMA1-RON2 interaction has no effect on the PfRh5-basigin Ca2+ flux but prevents host cytoskeleton disassembly. In contrast, the inhibition of parasite actin polymerisation had no effect on cytoskeletal clearance but caused a sustained Ca2+ response. We further demonstrate that establishment of the moving junction is temporally linked to clearance of the host cytoskeleton. Collectively, our findings support the existence of an association between the RON complex and components of the host cytoskeleton, which mediates the localised disruption of the erythrocyte-membrane cytoskeletal complex during invasion. ### Competing Interest Statement The authors have declared no competing interest. National Health and Medical Research Council, https://ror.org/011kf5r70, 2012271, 1117288, 1177431, 1121178, 1092789

bioRxiv

Rxiv mechanobio 2d ago

📰 "GAPMs form a heterotrimeric complex bridging the gliding machinery and the cytoskeleton across Plasmodium species"
https://www.biorxiv.org/content/10.64898/2026.03.27.714866v1?rss=1 #Cytoskeleton #Actomyosin #Dynamics

GAPMs form a heterotrimeric complex bridging the gliding machinery and the cytoskeleton across Plasmodium species

Apicomplexan parasites, such as malaria-causing Plasmodium spp., use a specialised actomyosin motor system known as the glideosome to drive movement through host tissue and invade host cells. This system is anchored to the inner membrane complex (IMC), a series of flattened vesicles located beneath the plasma membrane, and thought to be linked to the underlying cytoskeleton by the GAPM protein family. However, it is not known how these GAPM proteins are localised across the Plasmodium life cycle, and whether different family members function alone or together. Here, we show that in two Plasmodium species GAPM2 is an IMC component whose recruitment and organisation are tightly coordinated with nuclear and cytoskeletal dynamics during parasite replication and differentiation. We find that the GAPM2 interactome remodels between asexual and sexual stages using mass spectrometry. To understand the molecular relationship between three GAPM paralogues, we solved a cryo-electron microscopy structure of the GAPM complex. This revealed an obligate heterotrimeric architecture that forms an asymmetric platform, likely to serve as a docking interface for other components of the glideosome. Finally integrating our GAPM heterotrimer structure with mass spectrometry data allowed us to propose a unified structural model of the glideosome that is conserved across apicomplexan parasites. ### Competing Interest Statement The authors have declared no competing interest. Wellcome Trust, 225292/Z/22/Z, 225844/Z/22/Z Royal Society, https://ror.org/03wnrjx87, URF\R1\211567 UK Research and Innovation, https://ror.org/001aqnf71, EP/Y036158/1 Medical Research Council, MR/K011782/1 Biotechnology and Biological Sciences Research Council, https://ror.org/00cwqg982, BB/L013827/1, BB/X014681/1 European Research Council, https://ror.org/0472cxd90, EP/X024776/1

bioRxiv

Rxiv cytoskeleton 2d ago

📰 "GAPMs form a heterotrimeric complex bridging the gliding machinery and the cytoskeleton across Plasmodium species"
https://www.biorxiv.org/content/10.64898/2026.03.27.714866v1?rss=1
#Cytoskeleton #Actomyosin

GAPMs form a heterotrimeric complex bridging the gliding machinery and the cytoskeleton across Plasmodium species

Apicomplexan parasites, such as malaria-causing Plasmodium spp., use a specialised actomyosin motor system known as the glideosome to drive movement through host tissue and invade host cells. This system is anchored to the inner membrane complex (IMC), a series of flattened vesicles located beneath the plasma membrane, and thought to be linked to the underlying cytoskeleton by the GAPM protein family. However, it is not known how these GAPM proteins are localised across the Plasmodium life cycle, and whether different family members function alone or together. Here, we show that in two Plasmodium species GAPM2 is an IMC component whose recruitment and organisation are tightly coordinated with nuclear and cytoskeletal dynamics during parasite replication and differentiation. We find that the GAPM2 interactome remodels between asexual and sexual stages using mass spectrometry. To understand the molecular relationship between three GAPM paralogues, we solved a cryo-electron microscopy structure of the GAPM complex. This revealed an obligate heterotrimeric architecture that forms an asymmetric platform, likely to serve as a docking interface for other components of the glideosome. Finally integrating our GAPM heterotrimer structure with mass spectrometry data allowed us to propose a unified structural model of the glideosome that is conserved across apicomplexan parasites. ### Competing Interest Statement The authors have declared no competing interest. Wellcome Trust, 225292/Z/22/Z, 225844/Z/22/Z Royal Society, https://ror.org/03wnrjx87, URF\R1\211567 UK Research and Innovation, https://ror.org/001aqnf71, EP/Y036158/1 Medical Research Council, MR/K011782/1 Biotechnology and Biological Sciences Research Council, https://ror.org/00cwqg982, BB/L013827/1, BB/X014681/1 European Research Council, https://ror.org/0472cxd90, EP/X024776/1

bioRxiv

Rxiv cytoskeleton 4d ago

📰 "Mechanosensitive feedback organizes cell shape and motion during hindbrain neuropore morphogenesis"
https://doi.org/doi:10.1016/j.cub.2026.02.068
https://pubmed.ncbi.nlm.nih.gov/41881011/
#Actomyosin

Rxiv mechanobio 4d ago

📰 "Mechanosensitive feedback organizes cell shape and motion during hindbrain neuropore morphogenesis"
https://doi.org/doi:10.1016/j.cub.2026.02.068
https://pubmed.ncbi.nlm.nih.gov/41881011/
#Morphogenesis #Actomyosin #Mechanical #Cell

Rxiv cytoskeleton 5d ago

📰 "Transient contractility attenuation reprograms epithelial cells into a protrusion-driven state that drives tissue fluidization"
https://www.biorxiv.org/content/10.64898/2026.03.23.713577v1?rss=1
#Actomyosin

Transient contractility attenuation reprograms epithelial cells into a protrusion-driven state that drives tissue fluidization

Collective cell migration drives tissue morphogenesis, repair and remodeling, and is often accompanied by transitions from solid-like to fluid-like states. While such tissue fluidization has been linked to physical parameters such as cell density, shape and activity, how it is actively regulated by mechano-chemical interplay remains unclear. Previous research has shown that transient attenuation of actomyosin contractility induces a transition from pulsatile, spatially confined motion to coherent, persistent long-range collective flow; however, the underlying cellular and signaling mechanisms remain unclear. Here we uncover the mechanistic basis by which transient perturbation of cell contractility reprograms the migration mode of confluent epithelial cells into a leader-like, fluidizing state, by combining kinase-reporter live imaging, force measurements and mathematical modeling. This transition arises from coordinated changes in cell morphology, mechanics, and signaling, including reduced cortical tension, enhanced cell-substrate adhesion and traction forces, and increased tissue deformability. At the signaling level, this process is accompanied by a rewiring of extracellular signal-regulated kinase (ERK)-mediated mechanotransduction toward a protrusion-coupled mode that sustains migration even under fully confluent conditions. Consistently, a multicellular computational model further demonstrates that protrusion-driven migration is sufficient to promote shape-velocity alignment and drive a transition from caged to flocking-like collective states. Together, our results identify transient mechanical relaxation as a trigger for an intrinsic leader-like state that fluidizes epithelial confluent tissues through coordinated remodeling of cytoskeletal, adhesive, and signaling systems. ### Competing Interest Statement The authors have declared no competing interest. Singapore Ministry of Education Academic Research Fund (AcRF) Tier 2, MOE-T2EP302230010 National Research Foundation, Singapore (NRF) under its Mid-sized Grant, NRF-MSG-20230001

bioRxiv

Rxiv cytoskeleton 5d ago

📰 "S100A4: A calcium-binding protein at the crossroads of cancer, fibrosis, and antiviral immunity"
https://doi.org/doi:10.1016/j.bbrc.2026.153655
https://pubmed.ncbi.nlm.nih.gov/41875701/
#Actomyosin

Rxiv cytoskeleton Mar 23

📰 "Glassy dynamics in active epithelia emerge from an interplay of mechanochemical feedback and crowding"
https://arxiv.org/abs/2511.05469
#Physics.Bio-Ph #Cond-Mat.Soft #Actomyosin

Glassy dynamics in active epithelia emerge from an interplay of mechanochemical feedback and crowding

Glassy dynamics in active biological cells remain a subject of debate, as cellular activity rarely slows enough for true glassy features to emerge. In this study, we address this paradox of glassy dynamics in epithelial cells by integrating experimental observations with an active vertex model. We demonstrate that while crowding is essential, it is not sufficient for glassy dynamics to emerge. A mechanochemical feedback loop (MCFL), mediated by cell shape changes through the contractile actomyosin network, is required to drive glass transition in dense epithelial tissues, as revealed via a crosstalk between actin-based cell clustering and dynamic heterogeneity in experiments. Incorporating MCFL into the vertex model reveals contrasting results from those previously predicted by theories -- we show that the MCFL can counteract cell division-induced fluidisation and enable glassy dynamics to emerge through active cell-to-cell communication. Furthermore, our analysis reveals, for the first time, the existence of novel collective mechanochemical oscillations that arise from the crosstalk of two MCFLs. Together, we demonstrate that an interplay between crowding and active mechanochemical feedback enables the emergence of glass-like traits and collective biochemical oscillations in epithelial tissues with active cell-cell contacts.

arXiv.org

Rxiv cytoskeleton Mar 20

📰 "Stress fiber traction force reshapes chromatin accessibility and YAP binding to direct diverse transcriptional programs in mesenchymal stem cells"
https://doi.org/doi:10.1016/j.mbm.2026.100178
https://pubmed.ncbi.nlm.nih.gov/41858407/
#Actomyosin

Rxiv mechanobio Mar 19

📰 "Molecular-scale, nonlinear actomyosin binding dynamics drive population-scale adaptation and evolutionary convergence"
https://arxiv.org/abs/2603.17183 #Physics.Bio-Ph #Actomyosin #Dynamics #Nlin.Ao #Myosin #Force

Molecular-scale, nonlinear actomyosin binding dynamics drive population-scale adaptation and evolutionary convergence

Biological actuators -- from myosin motors to muscles -- follow Hill's model where a dimensionless parameter $α$ captures the nonlinear coupling between contraction rate and force generation. Our prior work identified a characteristic $α^* = 3.85 \pm 2.32$ across natural muscles and showed that $α^*$ optimizes a power-efficiency tradeoff, potentially explaining its prevalence in nature. However, those results reflected short-term actuation tasks whereas phenotypic distributions in $α$ emerge over evolutionary timescales. Here, we use numerical simulations of self-propelled agents to explore how nonlinear actomyosin actuation (parameterized by $α$) shapes population dynamics. Agents of different $α$ compete for resources and reproduce with slight mutations. Without mutations, resource availability drives populations in $α$ toward distinct behaviors: under abundance or scarcity, specialized $α$ survive. However, with mutations and selection, populations evolve toward distributions centered around the characteristic $α^*$ observed in nature. Further, we show that the mutation rate $δ$ governs a balance between adaptability and robustness: large $δ$ generates instability and extinction, small $δ$ prevents feedback, while intermediate $δ$ enables long-term adaptability while remaining robust to short-term noise. Our results suggest that nonlinear actuation provides a general understanding of energy management in actomyosin systems across a wide range of timescales, ranging from the task-specific to evolutionary. These insights may guide the rational design of active materials with adaptive properties.

arXiv.org