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Stress granules and P-bodies are conserved cytoplasmic biomolecular condensates whose assembly and composition are well documented, but whose clearance mechanisms remain controversial or poorly described. Such understanding could provide new insight into how cells regulate biomolecular condensate formation and function, and identify therapeutic strategies in disease states where aberrant persistence of stress granules in particular is implicated. Here, I review and compare the contributions of chaperones, the cytoskeleton, post-translational modifications, RNA helicases, granulophagy and the proteasome to stress granule and P-body clearance. Additionally, I highlight the potentially vital role of RNA regulation, cellular energy, and changes in the interaction networks of stress granules and P-bodies as means of eliciting clearance. Finally, I discuss evidence for interplay of distinct clearance mechanisms, suggest future experimental directions, and suggest a simple working model of stress granule clearance. [ABSTRACT FROM AUTHOR]

[Display omitted] • 1. AFM-based biophysical measurements are performed on a neural cell. • 2. Exposure to high-dose carbon dots affects cellular mechanics and morphology. • 3. Actin filaments are disorganized in the cells after exposure to high-dose carbon dots. • 4. Biological studies validate the cytotoxic effects disclosed by AFM. • 5. AFM is a powerful biophysical tool for the study of cell-nanomaterials interactions. Understanding the cytotoxicity of fluorescent carbon dots (CDs) is crucial for their applications, and various biochemical assays have been used to study the effects of CDs on cells. Knowledge on the effects of CDs from a biophysical perspective is integral to the recognition of their cytotoxicity, however the related information is very limited. Here, we report that atomic force microscopy (AFM) can be used as an effective tool for studying the effects of CDs on cells from the biophysical perspective. We achieve this by integrating AFM-based nanomechanics with AFM-based imaging. We demonstrate the performance of this method by measuring the influence of CDs on living human neuroblastoma (SH-SY5Y) cells at the single-cell level. We find that high-dose CDs can mechanically induce elevated normalized hysteresis (energy dissipation during the cell deformation) and structurally impair actin skeleton. The nanomechanical change highly correlates with the alteration of actin filaments, indicating that CDs-induced changes in SH-SY5Y cells are revealed in-depth from the AFM-based biophysical aspect. We validate the reliability of the biophysical observations using conventional biological methods including cell viability test, fluorescent microscopy, and western blot assay. Our work contributes new and significant information on the cytotoxicity of CDs from the biophysical perspective. [ABSTRACT FROM AUTHOR]

[Display omitted] • Sc3+ is selected to replace V3+ and PAN is introduced to provide porous carbon substrate. • Sc bonds with oxygen to form ScO 6 , resulting in improved structural stability and kinetics. • PAN can induce a beneficial nitrogen-doped carbon skeleton with defects, resulting in enhanced electronic conductivity. • After cycling XRD/SEM confirms the stabilized porous carbon skeleton and improved crystal stability. • Ex-situ XRD analysis reveals the crystal volume change in Sc-3 is relatively slight but reversible. The poor structural stability and conductivity of Na 3 V 2 (PO 4) 3 (NVP) have been serious limitations to its development. In this paper, Sc3+ is selected to replace partial site of V3+ which can enhance its ability to bond with oxygen, forming the ScO 6 octahedral unit, resulting in improved structural stability and better kinetic properties for the NVP system. Moreover, due to the larger ionic radius of Sc3+ compared to V3+, moderate Sc3+ substitution can support the crystal framework as pillar ions and expand the migration channels for de-intercalation of Na+, thus efficiently promoting ionic conductivity. The introduction of polyacrylonitrile (PAN) to provide an N -doped porous carbon substrate is another key aspect. The low-cost carbon resource of PAN can induce a beneficial nitrogen-doped carbon skeleton with defects, enhancing electronic conductivity at the interface to reduce the polarization phenomenon. The established pore structure can serve as a buffer for unit cell deformation caused by Na+ migration. Furthermore, the enlarged specific surface area provides more active sites for electrolyte infiltration, improving the material utilization rate. The after cycling X-ray Diffraction/scanning electron microscope (XRD/SEM) further confirms the stabilized porous carbon skeleton and improved crystal stability of Sc-3 material. Ex-situ XRD analysis shows that the crystal volume change in the Sc-3 cathode is relatively slight but reversible during the charge/discharge process, indicating that Sc3+ doping plays a crucial role in stabilizing the unit cell structure. The hybrid Sc/VO 6 and PO 4 units jointly build a strong bone structure to resist stress and weaken deformation. Accordingly, the optimized Sc-3 sample reveals an initial capacity of 115.9 mAh/g at 0.1C, with a capacity retention of 78.6 % after 2000 cycles at 30C. The Sc-3//CHC full battery can release a capacity of 191.3 mAh/g at 0.05C, accompanied by successful illumination, showcasing its promising practical applications. [ABSTRACT FROM AUTHOR]

The neural tube, the embryonic precursor to the brain and spinal cord, begins as a flat sheet of epithelial cells, divided into non-neural and neural ectoderm. Proper neural tube closure requires that the edges of the neural ectoderm, the neural folds, to elevate upwards and fuse along the dorsal midline of the embryo. We have previously shown that members of the claudin protein family are required for the early phases of chick neural tube closure. Claudins are transmembrane proteins, localized in apical tight junctions within epithelial cells where they are essential for regulation of paracellular permeability, strongly involved in apical-basal polarity, cell-cell adhesion, and bridging the tight junction to cytoplasmic proteins. Here we explored the role of Claudin-3 (Cldn3), which is specifically expressed in the non-neural ectoderm. We discovered that depletion of Cldn3 causes folic acid-insensitive primarily spinal neural tube defects due to a failure in neural fold fusion. Apical cell surface morphology of Cldn3-depleted non-neural ectodermal cells exhibited increased membrane blebbing and smaller apical surfaces. Although apical-basal polarity was retained, we observed altered Par3 and Pals1 protein localization patterns within the apical domain of the non-neural ectodermal cells in Cldn3-depleted embryos. Furthermore, F-actin signal was reduced at apical junctions. Our data presents a model of spina bifida, and the role that Cldn3 is playing in regulating essential apical cell processes in the non-neural ectoderm required for neural fold fusion. [Display omitted] • Avian model of neural tube defects resembling human spina bifida. • Role of the tight junction protein Claudin-3 in fusion of the neural tube. • Effects of Claudin-3 in regulating apical protein localization patterns. [ABSTRACT FROM AUTHOR]

[Display omitted] • A strategy of constructing porous N -doped carbon framework to improve NVP is proposed. • TEA serves as acid binding agent to convert PAA into polyamide salts. • PI was synthesized and decomposed to construct a porous framework. • N -doped carbon with rich-defects benefits for the migration of Na+ and electrons. • The optimized PAA-NVP-1 exhibits superior sodium storage property. Generally, the transport of electrons and Na+ is seriously constrained in Na 3 V 2 (PO 4) 3 (NVP) due to intense interactions of V-O and P O bonds. Besides, polyamide acid (PAA) is hardly used in the sol–gel route due to insolubility. This work develops a facile liquid synthesis strategy based on modified PAA, achieving in-situ construction of a porous N -doped carbon framework with rich defects to improve the kinetics of NVP. The addition of triethylamine (TEA) reacts with carboxyls in PAA to achieve acid-base neutralization, turning PAA into polyamide salts with good solubility. The special morphology construction mechanism of this unique system was observed by ex-situ scanning electron microscopy (SEM) and Transmission electron microscopy (TEM). Specifically, PAA undergoes in-situ conversion into chain-like polyimide (PI) through a thermal polymerization mechanism during the pre-sintering process. Meanwhile, NVP precursors are evenly dispersed in the PI fibers, efficiently reducing the particle size. After the final treatment, the favorable porous carbon skeleton could be generated derived from the partial decomposition of PI, on which small active grains are in situ grown. The resulting N -doped carbon substrate contains rich defects, benefiting from the migration of Na+. Furthermore, the porous construction is conducive to alleviating the stress and strain generated by the high current impact, increasing the contact area between electrodes/electrolytes to improve the utilization efficiency of active substances. Comprehensively, the optimized samples exhibit a capacity of 82.1 mAh g−1 at 15C with a retention rate of 95.45 % after 350 cycles. It submits a capacity of 67.6 mAh g−1 at 90C and remains 52.2 mAh g−1 after 1500 cycles. Even in full cells, it reveals a value of 110.6 mAh g−1. This work guides the application of in-situ multiple modifications of polymers in electrode materials. [ABSTRACT FROM AUTHOR]

Click-Chemistry synergic MXene-functionalized flexible skeleton membranes achieved high-efficiency selective separation to artemisinin. [Display omitted] • Transport to specific molecule was achieved assisted by MXene laminated structure. • High stability for perm-selectivity of MIMs in mobile phase was achieved. • Click-chemistry drove to build dot-matrix imprinting units. • MIMs showed excellent antibacterial properties and sustainable reusability. Membrane-based technology with accurate-recognition and specific-transmission has been regarded as one of the most promising strategies in environmental protection and energy conservation. However, membrane technique still faces challenges of "trade-off effect" between high selectivity and permeation flux within organic-aqueous mixed matrix. Here, well-intergrown click-chemistry synergic MXene-functionalized flexible skeleton membranes has been prepared in this strategy, enabling size-exclusion&structure selectivity by uniform location array imprinting unit and transport performance towards specific medicinal molecules of artemisinin (Ars). The well-assembled ultrathin cascade-type MXene layer guarantees the narrow interlayer nanochannels and the flexible skeleton modified mesoporous SiO 2 nanoparticles provide active reaction platform for the construction of selective recognition space. The resulting membranes demonstrated outstanding selective separation performance with permeability factor that artesunate (Aru) /Ars and dihydro-artemisinin (d -Ars) / Ars of 3.17 and 2.89 and permeation flux of 1173.25 L·m−2·h−1·bar−1. Besides, combined with antibacterial durability, recycling performance, high separation performance in mobile phase stability of CMFMs, it is anticipated that this work hopefully opens a new avenue for efficient chiral separation to medicinal molecules, exhibiting broad potential for practical application. [ABSTRACT FROM AUTHOR]

The novel ternary Li–Cu–Zn alloy is not a simple mixture of Li–Cu and Li–Zn alloys. Its delithiation skeleton is composed of highly lithiophilic and stable "Li-inactive" CuZn and "Li-active" CuZn 5 phases, effectively suppressing dendrite formation and volume changes in lithium metal anode. [Display omitted] • Multiple alloying reactions in multicomponent Li-rich alloy were discovered for the first time and two new skeletons, i.e., CuZn and CuZn 5 were formed in the Li–Cu–Zn ternary alloy. • The CuZn 5 skeleton is "Li-active" and the CnZn skeleton is "Li-inactive", both of which exhibit superior lithiophilicity and structural stability. • Li–Cu–Zn ternary alloy can mitigate the huge volume change during cycling. • The synergistic effect of CuZn and CuZn 5 realizes a dendrite-free Li deposition behavior. Lithium (Li)-rich ternary alloy, comprising a multi-alloy phase as the built-in three-dimensional (3D) framework and a Li metal phase as a reversible Li reservoir, is a promising high-energy–density anode for rechargeable Li metal batteries. The introduction of metal/metalloid components to the alloy can effectively regulate Li deposition and maintain the dimensional integrity of the Li anode. Herein, the lithium–copper–zinc (Li–Cu–Zn) ternary alloy, as a new type of alloy anode, is synthesized via a facile thermal melting method. The fully delithiated 3D scaffold comprised two Cu–Zn alloy phases named CuZn and CuZn 5. These alloy phases exhibit higher lithiophilicity and structural stability than Li–Zn and Li–Cu alloys. Moreover, the CuZn phase is electrochemically inert, ensuring the geometric stability of the anode, while the CuZn 5 phase can readily undergo alloying reaction with Li to form the LiZn phase, thereby facilitating uniform Li nucleation and deposition. The hybridized multiphase alloy structure and specific energy storage mechanism of the Cu–Zn based alloy scaffold in the ternary alloy anode facilitate dendrite-free Li deposition and prolonged cycle lifetime. The Li metal full battery based on lithium iron phosphate (LiFePO 4) cathode exhibits high cycling stability with high-capacity retention of 95.4% after 1000 cycles at 1C. [ABSTRACT FROM AUTHOR]

The intestinal epithelium must absorb many nutrients and water while forming a barrier that is impermeable to pathogens present in the external environment. Concurrently to fulfill this dual role, the intestinal epithelium is challenged by a rapid renewal of cells and forces resulting from digestion. Hence, intestinal homeostasis requires precise control of tissue integrity, tissue renewal, cell polarity, and force generation/transmission. In this review, we highlight the contribution of the cell cytoskeleton- actin, microtubules, and intermediate filaments- to intestinal epithelium homeostasis. With a focus on enterocytes, we first discuss the role of these networks in the formation and maintenance of cell-cell and cell-matrix junctions. Then, we cover their role in intracellular trafficking related to the apicobasal polarity of enterocytes. Finally, we report on the cytoskeletal changes that occur during tissue renewal. In conclusion, the importance of the cytoskeleton in maintaining intestinal homeostasis is emerging, and we think this field will keep evolving. [ABSTRACT FROM AUTHOR]

[Display omitted] • Herein, a facile synthesis of NVP with porous carbon skeleton is proposed. • The porous construction can alleviate the stress and strain caused by the current impact through deformation. • Ex-situ EIS reveals the carbon skeleton can reduce the surface resistance to promote the de-intercalation of Na+. • The ex-situ XPS spectra at different potentials confirms the stabilized existence of V O C bonds. • The modified PC-NVP releases superior sodium storage property. Low electronic conductivity and poor properties at high rate have hindered the application of Na 3 V 2 (PO 4) 3 (NVP). Herein, a facile synthesis of NVP with porous carbon skeleton is proposed. Specifically, Na 2 CO 3 and glucose, acting as hard templates, are introduced to the precursors after initial firing stage, and Na 2 CO 3 particles are removed by flushing after the final heatment. Due to the thermal conductivity of Na 2 CO 3 , the secondary addition of glucose can generate distinctive graphitized porous carbon skeleton, which bonds well with the amorphous carbon coating to construct stable and conductive network. The porous construction can alleviate the stress and strain caused by the current impact through deformation. Furthermore, ex-situ EIS reveals the highly conductive carbon skeleton can significantly reduce the surface resistance and result in an increase of effective voltage to promote the de-intercalation of Na+. Moreover, the ex-situ X-ray photoelectron spectroscopy (XPS) at different potentials confirms the stabilized existence of V O C bonds. Benefiting from the unique carbon skeleton, the PC-NVP releases capacity of 116.9 mAh g−1 at 0.1C. Even at 120C, PC-NVP still exhibits a high capacity of 84.7 mAh g−1, retaining a value of 41.3 mAh g−1 after 16,000 cycles, corresponding to a low decay rate of 0.0032% per cycle. [ABSTRACT FROM AUTHOR]

In this paper we construct a tropical moduli space parametrizing roots of divisors on tropical curves. We study the relation between this space and the skeleton of Jarvis moduli space of nets of limit roots on stable curves. We show that the combinatorics of the moduli space of tropical roots is governed by the poset of flows, a poset parametrizing certain flows on graphs. [ABSTRACT FROM AUTHOR]

Low-intensity ultrasound can be applied for medical imaging and disease treatment in clinical and experimental studies. However, the biological effects of ultrasound on blood vessels, especially endothelial cells (ECs) are still unclear. In this study, the laws of endothelial cytoskeleton changes under ultrasound induction are investigated. ECs are exposed to low-intensity ultrasound, and the cytoskeletal morphology is analyzed by a filamentous (F)-actin staining technique. We further analyze the characteristics of cytoskeleton rupture using indirect immunofluorescence techniques and cytoskeleton electron microscopy. Finally, the biological effects induced by ultrasound at the tissue level are investigated in an ex vivo blood-vessel model. Significant changes in cytoskeletal structure are detected when induced by ultrasound, including cytoskeletal rupture, blebbing and apoptosis. Moreover, a temporal threshold of ECs injury under different ultrasonic intensities is established. This study illustrates a pattern of significant changes in the cytoskeletal structure of ECs induced by ultrasound. The finding serves as a guide for selecting a safe threshold for clinical ultrasound applications. • Phenomenon and signaling events of the endothelial cytoskeleton response to ultrasound are elucidated. • The time threshold of cell injury under low frequency ultrasonic induction is presented. • The ultrasound-induced injury at the vascular tissue level increases vascular permeability. [ABSTRACT FROM AUTHOR]

The virulence of SARS-CoV-2 decreases with increasing infectivity, the primary approaches for antiviral treatments will be preventing or minimizing the complications resulting from virus infection. ADAM metallopeptidase domain 17 (ADAM17) activation by SARS-CoV-2 infection has a dual effect on the development of the disease: increased release of inflammatory cytokines and dysregulation of Angiotensin converting enzyme II (ACE2) on cell surfaces, inflammatory cytokine infiltration and loss of ACE2 protective function lead to a significant increase in the incidence of related complications. Importantly, pathologically activated ADAM17 showed superior features than S protein in regulating ACE2 expression and participating in the intra cellular replication of SARS-CoV-2. In short, SARS-CoV-2 elicits only a limited immune response when it promotes its own replication and pathogenicity through ADAM17. Therefore, the pathological activation of ADAM17 may also represent a diminished innate antiviral defense and an altered strategy of SARS-CoV-2 infection. In this review, we summarized recent advances in our understanding of the pathophysiology of ADAM17, with a focus on the new findings that SARS-CoV-2 affects ADAM17 expression through Furin protein converting enzyme and Mitogen-activated protein kinase (MAPK) pathway, and raises the hypothesis that SARS-CoV-2 may mediates the pathological activation of ADAM17 by hijacking the actin regulatory pathway, and discussed the underlying biological principles. • The complications induced by SARS-CoV-2 infection are related to pathological activation of ADAM17 • The mechanism of pathological activation of ADAM17 by SARS-CoV-2 remains unclear • The role of actin cytoskeleton in SARS-CoV-2 infection was hypothesized [ABSTRACT FROM AUTHOR]

[Display omitted] • Increased surface area, mesopore abundance boost active sites, enhance charge transfer, and facilitate ion transport. • Interfacial electron transfer induces local water dissociation for optimized OER and HER kinetics. • CoMoO 4 enhances thermal stability, preventing carbon skeleton collapse and active site agglomeration in CoMoO4-CoP/NC during annealing. We report the synthesis and electrocatalytic properties of a CoMoO 4 -CoP heterostructure anchored on a hollow polyhedral N -doped carbon skeleton (CoMoO 4 -CoP/NC) for water-splitting applications. The preparation involved the anion exchange of MoO 4 2- to the organic ligand of ZIF-67, the self-hydrolysis of MoO 4 2-, and NaH 2 PO 2 phosphating annealing. CoMoO 4 was found to enhance thermal stability and prevent active site agglomeration during annealing, while the hollow structure of CoMoO 4 -CoP/NC provided a large specific surface area and high porosity that facilitated mass transport and charge transfer. The interfacial electron transfer from Co to Mo and P sites promoted the generation of electron-deficient Co sites and electron-enriched P sites, which accelerated water dissociation. CoMoO 4 -CoP/NC exhibited excellent electrocatalytic activity for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) in 1.0 M KOH solution, with overpotentials of 122 mV and 280 mV at 10 mA cm−2, respectively. The CoMoO 4 -CoP/NC‖CoMoO 4 -CoP/NC two-electrode system only required an overall water splitting (OWS) cell voltage of 1.62 V to achieve 10 mA cm−2 in an alkaline electrolytic cell. In addition, the material showed comparable activity to 20% Pt/C‖RuO 2 in a pure water home-made membrane electrode device, demonstrating potential for practical applications in proton exchange membrane (PEM) electrolyzers. Our results suggest that CoMoO 4 -CoP/NC is a promising electrocatalyst for efficient and cost-effective water splitting. [ABSTRACT FROM AUTHOR]

Tubular epithelial cells are routinely exposed to severe changes in osmolarity. Although the autophagic activity of cells is an indispensable process to maintain cellular homeostasis and respond to stressors, the effect of hyperosmotic stress on autophagic activity in tubular epithelial cells remains unknown. The aim of this study was to determine the effect of hyperosmotic stress on autophagy in rat kidney tubular epithelial cells focusing on the role of actin and microtubule cytoskeletons. Normal rat kidney (NRK)-52E cells exposed to mannitol-induced hyperosmotic stress. As a result, NRK-52E cells showed elevated protein levels of the autophagosome marker LC3-II, indicating enhancement of the autophagic flux. Hyperosmotic stress also transiently decreased cell volume and caused the reorganization of actin and microtubule cytoskeletal structures in NRK-52E cells. The inhibition of the actin cytoskeleton reorganization by cytochalasin D impaired the increase in the levels of LC3-II; however, disassembly of the microtubules following treatment with nocodazole did not affect the increase. These results indicate that hyperosmotic stress can induce autophagy mediated by the reorganization of the actin cytoskeleton in tubular epithelial cells. • Hyperosmotic stress enhances autophagic flux in proximal tubular epithelial cells. • Transient cell volume reduction by hyperosmolarity causes actin reorganization. • Inhibition of actin reorganization impairs the hyperosmolarity-induced autophagy. [ABSTRACT FROM AUTHOR]

[Display omitted] • The fabricated Fe-Ni-HPCNF has hierarchical porous skeleton and Fe/Ni-N catalytic sites. • Fe-Ni-HPCNF modified cell shows shuttle inhibition and kinetics promotion. • It sheds new light for the design of anti-self-discharged lithium-sulfur batteries. Lithium-sulfur (Li-S) batteries are featured with high gravimetric energy density, yet their commercial application is significantly deteriorated with the severe self-discharging resulted from the polysulfides shuttle and sluggish electrochemical kinetics. Here, a hierarchical porous carbon nanofibers implanted with Fe/Ni-N (denoted as Fe-Ni-HPCNF) catalytic sites are prepared and used as a kinetics booster toward anti-self-discharged Li-S batteries. In this design, the Fe-Ni-HPCNF possesses interconnected porous skeleton and abundant exposed active sites, enabling fast Li-ion conduction, excellent shuttle inhibition and catalytic ability for polysulfides' conversion. Combined with these advantages, this cell with the Fe-Ni-HPCNF equipped separator exhibits an ultralow self-discharged rate of 4.9% after resting for one week. Moreover, the modified batteries deliver a superior rate performance (783.3 mAh g−1 at 4.0 C) and an outstanding cycling life (over 700 cycles with 0.057% attenuation rate at 1.0 C). This work may guide the advanced design of anti-self-discharged Li-S batteries. [ABSTRACT FROM AUTHOR]

Cell division and cytoskeleton organization are fundamental processes participating in the development of Drosophila imaginal discs. In this manuscript we describe the phenotypes in the adult fly wing generated by knockdowns of 85% of Drosophila genes encoding proteins likely related to the regulation of cell division and cytoskeleton organization. We also compile a molecular classification of these proteins into classes that describe their expected or known main biochemical characteristics, as well as mRNA expression in the wing disc and likely protein subcellular localization for a subset of these genes. Finally, we analyze in more detail one protein family of cytoskeleton genes (Arp2/3 complex), and define the consequences of interfering with cell division for wing growth and patterning. [Display omitted] • We studied Drosophila wing phenotypes of cell division and the cytoskeleton genes. • Cell division and cytoskeletal genes affect mainly wing size. • The Arp2/3 complex influences cell division and survival in epithelial cells. • An identical venation pattern is accommodated into extremely different wing sizes. [ABSTRACT FROM AUTHOR]

Fibroblasts play an important role in maintaining tissue integrity by secreting components of the extracellular matrix and initiating response to injury. Although the function of fibroblasts has been extensively studied in adults, the embryonic origin and diversification of different fibroblast subtypes during development remain largely unexplored. Using zebrafish as a model, we show that the sclerotome, a sub-compartment of the somite, is the embryonic source of multiple fibroblast subtypes including tenocytes (tendon fibroblasts), blood vessel associated fibroblasts, fin mesenchymal cells, and interstitial fibroblasts. High-resolution imaging shows that different fibroblast subtypes occupy unique anatomical locations with distinct morphologies. Long-term Cre-mediated lineage tracing reveals that the sclerotome also contributes to cells closely associated with the axial skeleton. Ablation of sclerotome progenitors results in extensive skeletal defects. Using photoconversion-based cell lineage analysis, we find that sclerotome progenitors at different dorsal-ventral and anterior-posterior positions display distinct differentiation potentials. Single-cell clonal analysis combined with in vivo imaging suggests that the sclerotome mostly contains unipotent and bipotent progenitors prior to cell migration, and the fate of their daughter cells is biased by their migration paths and relative positions. Together, our work demonstrates that the sclerotome is the embryonic source of trunk fibroblasts as well as the axial skeleton, and local signals likely contribute to the diversification of distinct fibroblast subtypes. [Display omitted] • The sclerotome is the embryonic source of distinct fibroblasts in zebrafish. • The sclerotome contributes to the proper development of the axial skeleton. • The sclerotome mostly contains unipotent and bipotent progenitors. • Sclerotome differentiation is biased by the axial position and migratory path. [ABSTRACT FROM AUTHOR]

The axon is a sophisticated macromolecular machine composed of interrelated parts that transmit signals like spur gears transfer motion between parallel shafts. The growth cone is a fine sensor that integrates mechanical and chemical cues and transduces these signals through the generation of a traction force that pushes the tip and pulls the axon shaft forward. The axon shaft, in turn, senses this pulling force and transduces this signal in an orchestrated response, coordinating cytoskeleton remodeling and intercalated mass addition to sustain and support the advancing of the tip. Extensive research suggests that the direct application of active force is per se a powerful inducer of axon growth, potentially bypassing the contribution of the growth cone. This review provides a critical perspective on current knowledge of how the force is a messenger of axon growth and its mode of action for controlling navigation, including aspects that remain unclear. It also focuses on novel approaches and tools designed to mechanically manipulate axons, and discusses their implications in terms of potential novel therapies for re-wiring the nervous system. [ABSTRACT FROM AUTHOR]

Axon growth enables the rapid wiring of the central nervous system. Understanding this process is a prerequisite to retriggering it under pathological conditions, such as a spinal cord injury, to elicit axon regeneration. The last decades saw progress in understanding the mechanisms underlying axon growth. Most of these studies employed cultured neurons grown on flat surfaces. Only recently studies on axon growth were performed in 3D. In these studies, physiological environments exposed more complex and dynamic aspects of axon development. Here, we describe current views on axon growth and highlight gaps in our knowledge. We discuss how axons interact with the extracellular matrix during development and the role of the growth cone and its cytoskeleton within. Finally, we propose that the time is ripe to study axon growth in a more physiological setting. This will help us uncover the physiologically relevant mechanisms underlying axon growth, and how they can be reactivated to induce axon regeneration. [ABSTRACT FROM AUTHOR]

Morphogenesis of the nervous system involves a highly complex spatio-temporal pattern of physical forces (mainly tension and pressure) acting on cells and tissues that are pliable but have an intricately organized cytoskeletal infrastructure. This review begins by covering basic principles of biomechanics and the core cytoskeletal toolkit used to regulate the shapes of cells and tissues during embryogenesis and neural development. It illustrates how the principle of 'tensegrity' provides a useful conceptual framework for understanding how cells dynamically respond to forces that are generated internally or applied externally. The latter part of the review builds on this foundation in considering the development of mammalian cerebral cortex. The main focus is on cortical expansion and folding – processes that take place over an extended period of prenatal and postnatal development. Cortical expansion and folding are likely to involve many complementary mechanisms, some related to regulating cell proliferation and migration and others related to specific types and patterns of mechanical tension and pressure. Three distinct multi-mechanism models are evaluated in relation to a set of 18 key experimental observations and findings. The Composite Tension Plus (CT+) model is introduced as an updated version of a previous multi-component Differential Expansion Sandwich Plus (DES+) model (Van Essen, 2020); the new CT+ model includes 10 distinct mechanisms and has the greatest explanatory power among published models to date. Much needs to be done in order to validate specific mechanistic components and to assess their relative importance in different species, and important directions for future research are suggested. • Mechanical tension mediated by the cytoskeleton plays a key role in many aspects of morphogenesis. • Expansion and folding of cerebral cortex are key to achieving a large cortical surface area while keeping wiring compact. • The Composite Tension Plus (CT+) model invokes 10 distinct mechanisms to account for cortical expansion and folding. [ABSTRACT FROM AUTHOR]

Much of the focus of neuronal cell biology has been devoted to growth cone guidance, synaptogenesis, synaptic activity, plasticity, etc. The axonal shaft too has received much attention, mainly for its astounding ability to transmit action potentials and the transport of material over long distances. For these functions, the axonal cytoskeleton and membrane have been often assumed to play static structural roles. Recent experiments have changed this view by revealing an ultrastructure much richer in features than previously perceived and one that seems to be maintained at a dynamic steady state. The role of mechanics in this is only beginning to be broadly appreciated and appears to involve passive and active modes of coupling different biopolymer filaments, filament turnover dynamics and membrane biophysics. Axons, being unique cellular processes in terms of high aspect ratios and often extreme lengths, also exhibit unique passive mechanical properties that might have evolved to stabilize them under mechanical stress. In this review, we summarize the experiments that have exposed some of these features. It is our view that axonal mechanics deserves much more attention not only due to its significance in the development and maintenance of the nervous system but also due to the susceptibility of axons to injury and neurodegeneration. [ABSTRACT FROM AUTHOR]

Normal axon development depends on the action of mechanical forces both generated within the cytoskeleton and outside the cell, but forces of large magnitude or rate cause damage instead. Computational models aid scientists in studying the role of mechanical forces in axon growth and damage. These studies use simulations to evaluate how different sources of force generation within the cytoskeleton interact with each other to regulate axon elongation and retraction. Furthermore, mathematical models can help optimize externally applied tension to promote axon growth without causing damage. Finally, scientists also use simulations of axon damage to investigate how forces are distributed among different components of the axon and how the tissue surrounding an axon influences its susceptibility to injury. In this review, we discuss how computational studies complement experimental studies in the areas of axon growth, regeneration, and damage. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the major pathophysiological basis of a variety of cardiovascular diseases and has been recognized as a lipid-driven chronic inflammatory disease. Gelsolin (GSN) is a member of the GSN family. The main function of GSN is to cut and seal actin filaments to regulate the cytoskeleton and participate in a variety of biological functions, such as cell movement, morphological changes, metabolism, apoptosis and phagocytosis. Recently, more and more evidences have demonstrated that GSN is Closely related to atherosclerosis, involving lipid metabolism, inflammation, cell proliferation, migration and thrombosis. This article reviews the role of GSN in atherosclerosis from inflammation, apoptosis, angiogenesis and thrombosis. • This paper introduces the comprehensive structure, function, and distribution of GSN in the body. • Evidence gathered for link between GSN and pathological basis of atherosclerosis. • On the basis of research, it is speculated that the target of GSN on atherosclerosis. • Proposes the possibility of GSN as a biomarker for atherosclerosis. [ABSTRACT FROM AUTHOR]

Of all the cell types arising from the neural crest, ectomesenchyme is likely the most unusual. In contrast to the neuroglial cells generated by neural crest throughout the embryo, consistent with its ectodermal origin, cranial neural crest-derived cells (CNCCs) generate many connective tissue and skeletal cell types in common with mesoderm. Whether this ectoderm-derived mesenchyme (ectomesenchyme) potential reflects a distinct developmental origin from other CNCC lineages, and/or epigenetic reprogramming of the ectoderm, remains debated. Whereas decades of lineage tracing studies have defined the potential of CNCC ectomesenchyme, these are being revisited by modern genetic techniques. Recent work is also shedding light on the extent to which intrinsic and extrinsic cues determine ectomesenchyme potential, and whether maintenance or reacquisition of CNCC multipotency influences craniofacial repair. • Cranial neural crest provides a vertebrate-specific source of head mesenchyme. • Epigenetic reprogramming facilitates mesenchyme potential of neural crest. • Region- and species-specific contributions of ectomesenchyme to diverse cell types. • Plasticity of neural crest and mesoderm to contribute to craniofacial mesenchyme. • Unclear potential of cranial neural crest cells for enhanced skeletal repair. [ABSTRACT FROM AUTHOR]

[Display omitted] Cytotoxicity of nanoparticles is routinely characterized by biochemical assays such as cell viability and membrane integrity assays. However, these approaches overlook cellular biophysical properties including changes in the actin cytoskeleton, cell stiffness, and cell morphology, particularly when cells are exposed to "non-cytotoxic" doses of nanoparticles. Zeolitic imidazolate framework-8 nanoparticles (ZIF-8 NPs), a member of metal–organic framework family, has received increasing interest in various fields such as environmental and biomedical sciences. ZIF-8 NPs may enter the blood circulation system after unintended oral and inhalational exposure or intended intravenous injection for diagnostic and therapeutic applications, yet the effect of ZIF-8 NPs on vascular endothelial cells is not well understood. Here, the biophysical impact of "non-cytotoxic" dose ZIF-8 NPs on human aortic endothelial cells (HAECs) is investigated. We demonstrate that "non-cytotoxic" doses of ZIF-8 NPs, pre-defined by a series of biochemical assays, can increase the endothelial permeability of HAEC monolayers by causing cell junction disruption and intercellular gap formation, which can be attributed to actin reorganization within adjacent HAECs. Nanomechanical atomic force microscopy and super resolution fluorescence microscopy further confirm that "non-cytotoxic" doses of ZIF-8 NPs change the actin structure and cell morphology of HAECs at the single cell level. Finally, the underlying mechanism of actin reorganization induced by the "non-cytotoxic" dose ZIF-8 NPs is elucidated. Together, this study indicates that the "non-cytotoxic" doses of ZIF-8 NPs, intentionally or unintentionally introduced into blood circulation, may still pose a threat to human health, considering increased endothelial permeability is essential to the progression of a variety of diseases. From a broad view of cytotoxicity evaluation, it is important to consider the biophysical properties of cells, since they can serve as novel and more sensitive markers to assess nanomaterial's cytotoxicity. [ABSTRACT FROM AUTHOR]

The organ of Corti, located in the cochlea within the inner ear is the receptor organ for hearing. It converts auditory signals into neuronal action potentials that are transmitted to the brain for further processing. The mature organ of Corti consists of a variety of highly differentiated sensory cells that fulfil unique tasks in the processing of auditory signals. The actin and microtubule cytoskeleton play essential function in hearing, however so far, more attention has been paid to the role of actin. Microtubules play important roles in maintaining cellular structure and intracellular transport in virtually all eukaryotic cells. Their functions are controlled by interactions with a large variety of microtubule-associated proteins (MAPs) and molecular motors. Current advances show that tubulin posttranslational modifications, as well as tubulin isotypes could play key roles in modulating microtubule properties and functions in cells. These mechanisms could have various effects on the stability and functions of microtubules in the highly specialised cells of the cochlea. Here, we review the current understanding of the role of microtubule-regulating mechanisms in the function of the cochlea and their implications for hearing, which highlights the importance of microtubules in the field of hearing research. [ABSTRACT FROM AUTHOR]

[Display omitted] Transition metal oxides have shown high theoretical capacities as anode materials and have been considered as high potential materials to substitute graphite for composing new generations of lithium-ion batteries (LIBs). However, the considerable volume changes of transition metal oxide materials during practical processes have limited their applications. Herein, we report a simple approach to construct a two-dimensional (2D) hollow carbon skeleton decorated with ultrafine Co 3 O 4 nanoparticles (Co 3 O 4 /C). This composite is derived from a leaf-like zeolitic imidazolate framework-L (ZIF-L (Co)) via etching coordination using tannic acid (TA). The Co 3 O 4 /C has a unique structure consisting of 2D carbon skeleton, ultrafine Co 3 O 4 nanoparticle, and open channel, which can accelerate electron transport, alleviate volume change, and facilitate ion diffusion. Benefiting from these features, the LIBs assembled using Co 3 O 4 /C as anode material exhibits superior reversible cycle performance and impressive rate property. This study provides an efficient strategy for implementing transition metal oxide-based composites for energy storage applications. [ABSTRACT FROM AUTHOR]

A plate-like Bi/Bi 2 O 3 -C heterostructure with boosted potassium storage performances is designed through a MOF-derived structure-inheritance strategy, where the Bi and Bi 2 O 3 can form hetero-particles that are uniformly embedded within the MOF-derived carbon skeleton. [Display omitted] Bismuth-based materials are regarded as promising anode materials for potassium ion batteries (PIBs) due to their high theoretical capacity and low working potential. However, the large volume expansion and sluggish kinetics during cycling are major limitations to their practical application. Herein, a unique Bi/Bi 2 O 3 -C heterostructure was designed through a simple Bi-metal–organic framework (MOF) modulation-pyrolysis process. X-ray photoelectron spectroscopy, transmission electron microscopy, and X-ray diffraction revealed that the Bi and Bi 2 O 3 can form hetero-particles, which were uniformly embedded in a plate-like carbon skeleton, constructing a Bi/Bi 2 O 3 -C heterostructure. The carbon skeleton and the formation of numerous hetero-interfaces between Bi, Bi 2 O 3 , and carbon can effectively promote the interfacial charge transfer, shorten the K+ diffusion pathway, and alleviate the volume expansion of Bi/Bi 2 O 3 during potassiation. Consequently, the Bi/Bi 2 O 3 -C heterostructure exhibited a high reversible capacity of 426.0 mAh g−1 at 50 mA g−1, excellent cycle performance of 251.8 mAh g−1 after 350 cycles with a capacity retention of 76.6 %, and superior rate capability of 82.7 mAh g−1 at 1 A g−1, demonstrating its promising potential for the application of PIBs anode. [ABSTRACT FROM AUTHOR]

A plate-like Bi/Bi 2 O 3 -C heterostructure with boosted potassium storage performances is designed through a MOF-derived structure-inheritance strategy, where the Bi and Bi 2 O 3 can form hetero-particles that are uniformly embedded within the MOF-derived carbon skeleton. [Display omitted] Bismuth-based materials are regarded as promising anode materials for potassium ion batteries (PIBs) due to their high theoretical capacity and low working potential. However, the large volume expansion and sluggish kinetics during cycling are major limitations to their practical application. Herein, a unique Bi/Bi 2 O 3 -C heterostructure was designed through a simple Bi-metal–organic framework (MOF) modulation-pyrolysis process. X-ray photoelectron spectroscopy, transmission electron microscopy, and X-ray diffraction revealed that the Bi and Bi 2 O 3 can form hetero-particles, which were uniformly embedded in a plate-like carbon skeleton, constructing a Bi/Bi 2 O 3 -C heterostructure. The carbon skeleton and the formation of numerous hetero-interfaces between Bi, Bi 2 O 3 , and carbon can effectively promote the interfacial charge transfer, shorten the K+ diffusion pathway, and alleviate the volume expansion of Bi/Bi 2 O 3 during potassiation. Consequently, the Bi/Bi 2 O 3 -C heterostructure exhibited a high reversible capacity of 426.0 mAh g−1 at 50 mA g−1, excellent cycle performance of 251.8 mAh g−1 after 350 cycles with a capacity retention of 76.6 %, and superior rate capability of 82.7 mAh g−1 at 1 A g−1, demonstrating its promising potential for the application of PIBs anode. [ABSTRACT FROM AUTHOR]

[Display omitted] • The morphology of hollow nanoprisms N -Co-Cu-S-x HNs synthesized by the self-templating method can be controlled. • Cu was successfully introduced to modulate the electronic structure of the Co center to improve the electrical conductivity. • The N -containing C skeleton protects internal active sites of the catalysts to stabilize the OER activity. • N -CoCu-S-0.25 exhibits exciting catalytic activity and durability (27 h). CoS x materials with high catalytic activity are considered as promising HER electrocatalysts, but their inherent low electrical conductivity and easy loss of active sites have greatly limited their applications in OER electrocatalysis. Herein, we present a convenient method to synthesize Co-Cu hollow nanoprisms after wrapping and calcining with trithiocyanuric acid (C 3 H 3 N 3 S 3) (denoted N -Co-Cu-S-x HNs). The results showed that Cu doping modified the charge density of Co center, leading to the enhancement of the intrinsic activity of the Co 3 S 4 active center, meanwhile wrapping trithiocyanuric acid on the surfaces and calcinating to form N -containing C skeleton as a flexible substrate to encapsulate the catalysts, which effectively protected the active sites inside the catalysts. Notably, the OER catalyst that was optimized by adjusting the metal ratio and controlling the trithiocyanuric acid incorporation exhibited a low overpotential of 306 mV under a current density of 10 mA cm−2 and showed a superior durability of more than 27 h. This work may provide some insights into the preparation of oxygen evolution reaction catalysts with excellent performance through doping transition metals and protecting the internal active sites strategies. [ABSTRACT FROM AUTHOR]

Actin is an integral component of the cytoskeleton, which plays an important role in various fundamental cellular processes, such as affecting the polarity of embryonic cells during embryonic development in various model organisms. Meanwhile, previous studies have demonstrated that the polymerization of the actin cytoskeleton can affect cell migration, proliferation, and differentiation. Actin polymerization state regulated osteogenic differentiation and affected cell proliferation. However, the function of actin in regenerative biology has not been thoroughly elucidated. The planarian flatworm, which contains a large number of adult somatic stem cells (neoblasts), is an ideal model organism to study regenerative biology. Here, we identified a homolog of actin in planarian Dugesia japonica and found that RNAi targeting actin during planarian regeneration results in the formation of protrusions on the dorsal side, where the division of phospho-H3 mitotic cells is increased. In addition, a decrease in differentiation is observed in regenerating tissues after Djactin RNAi. These results indicate that Djactin functions in proliferation and differentiation control in planarian regeneration. • Actin is required for planarian regeneration by regulating proliferation and differentiation control. • Actin RNAi induces stem cell hyper-proliferation and results in the formation of protrusions. • Inhibition actin decreases the differentiation in regenerating tissues. [ABSTRACT FROM AUTHOR]

During morphogenesis, changes in the shapes of individual cells are harnessed to mold an entire tissue. These changes in cell shapes require the coupled remodeling of the plasma membrane and underlying actin cytoskeleton. In this review, we highlight cellularization of the Drosophila embryo as a model system to uncover principles of how membrane and actin dynamics are co-regulated in space and time to drive morphogenesis. [ABSTRACT FROM AUTHOR]

Charles Breder, a pioneering researcher of blind Mexican cavefish was the first to note extreme variation in the facial skeleton of this intriguing subterranean-dwelling organism. Using a system of polar coordinate plots, he identified substantial dysmorphic changes affecting bones of the orbital skeleton. A complication of his landmark publication from 1944 was an error in the number of orbital bones depicted for this species. Intriguingly, however, he proposed an unknown "organizing force" likely influences final bone position and associated dysmorphia. At the time this was merely hypothetical. Roughly eight decades since its publication, however, insights into sensory influences on facial bone development may explain dysmorphia and variation in bone numbers for Astyanax cavefish. A morphological association between mechano-sensory neuromasts of the lateral line and dermal bones of the facial skeleton had been appreciated in the classical literature, but the polarity of this interaction has long remained unclear. Here, we propose that sensory-skeletal integration between sensory neuromasts and bones explain the incomplete numbers of bones, and dysmorphic features such as fusion between neighboring elements. We propose that in closely-related surface fish (and most teleost fish) this developmental coupling enables the sensory and skeletal systems to become integrated into a functional unit over the course of life history. In this opinion article, we discuss the relevance of this (poorly understood) phenomenon as a potential evolutionary source of variation in the facial bone structures of taxa across deep geologic time. We provide three potential explanations for the error in Breder's drawings, that may be explained by natural developmental variation documented in other related species. Moreover, we argue that the natural variation in this "evolutionary" model system is useful for explaining diverse cranial features by uniting aberrations occurring during embryogenesis with long-term adult dysmorphia. [Display omitted] • Charles Breder represented Astyanax as having too few orbital bones. • Breder proposed an "unknown organizing force" governed development of these bones. • This "force" is likely the osteogenic capacity of sensory neuromasts. • Sensory neuromasts likely induce bone to prefigure their functional role. • Variations on sensory-skeletal integration explain aberrations in cavefish. [ABSTRACT FROM AUTHOR]

Ethanol is a known vertebrate teratogen that causes craniofacial defects as a component of fetal alcohol syndrome (FAS). Our results show that sea urchin embryos treated with ethanol similarly show broad skeletal patterning defects, potentially analogous to the defects associated with FAS. The sea urchin larval skeleton is a simple patterning system that involves only two cell types: the primary mesenchymal cells (PMCs) that secrete the calcium carbonate skeleton and the ectodermal cells that provide migratory, positional, and differentiation cues for the PMCs. Perturbations in RA biosynthesis and Hh signaling pathways are thought to be causal for the FAS phenotype in vertebrates. Surprisingly, our results indicate that these pathways are not functionally relevant for the teratogenic effects of ethanol in developing sea urchins. We found that developmental morphology as well as the expression of some ectodermal and PMC genes was delayed by ethanol exposure. Temporal transcriptome analysis revealed significant impacts of ethanol on signaling and metabolic gene expression, and a disruption in the timing of GRN gene expression that includes both delayed and precocious gene expression throughout the specification network. We conclude that the skeletal patterning perturbations in ethanol-treated embryos likely arise from a loss of temporal synchrony within and between the instructive and responsive tissues. [Display omitted] • Ethanol perturbs sea urchin skeletal patterning. • Ethanol-mediated phenotypes are not mediated by retinoic acid. • Ethanol desynchronizes specification network gene expression timing. [ABSTRACT FROM AUTHOR]

Cell migration is a cytoskeleton-driven cellular process involved in physiological and pathological events such as embryonic development and cancer metastasis. Fibroblasts have often been used to elucidate the mechanism of cell migration due to their high morphological polarity and migratory activity. We recently reported that human lung fibroblasts migrate straight for a long duration without external stimuli, which phenomenon we named intrinsic and directed migration (IDM) of fibroblasts. In this study, we explored proteins involved in IDM in order to elucidate the molecular mechanism. First, we focused on the differences in morphology and migratory behaviors between normal and immortalized fibroblasts—the former exhibit obvious polarity and IDM; the latter exhibit poorly polarized morphology and random migration. We compared the abundance of proteins functioning as the cytoskeletal components between them through proteomic analysis and found that LIM domain only protein 7 (LMO7) is overwhelmingly incorporated into the cytoskeletons of normal fibroblasts. Depletion of LMO7 inhibited the directed migration of normal fibroblast on the fibronectin (FN)-rich surface, suggesting that LMO7 is important for IDM. Moreover, on the FN-free surface, LMO7-depleted fibroblasts often failed to establish morphological polarity and hardly migrated. Thus, the present study identified LMO7 as a positive regulator of fibroblast polarization and IDM, especially in an environment where integrin-mediated substrate attachment is insufficient. • LMO7 is abundant in the cytoskeletal fraction of normal fibroblasts. • LMO7 is critical for the proper polarization and migration of fibroblasts. • The significance of LMO7 on fibroblast migration depends on the ECM condition. [ABSTRACT FROM AUTHOR]

[Display omitted] • Design and manufacture of Ni/MoO 2 catalysts with different morphologies, which confirm the effect of morphology engineering. • The excellent catalytic performance of H-Ni/MoO 2 benefits from a hollow porous spherical structure with amorphous carbon skeleton, compared with other morphological Ni/MoO 2. • The urea plays crucial role in porous hollow spherical morphology and carbon skeleton in the synthesized steps. • The urea-assistant synthesized way offers a simple and practical strategy to construct this structure for catalysts. The catalyst morphology has a strong impact on the activity of electrocatalytic hydrogen production. Considering the effect, we design and fabricate hollow spherical Ni/MoO 2 heterojunction. In addition, an amorphous carbon skeleton is inserted into the hollow sphere, which makes the structure more stable and porous. Compared with other morphological Ni/MoO 2 , the porous hollow spherical Ni/MoO 2 (H-Ni/MoO 2) with an internal carbon skeleton shows better hydrogen evolution reaction (HER) activity with a small overpotential of 58 mV to reach 10 mA cm−2 and a tafel value of 44.8 mV dec-1 in alkaline media. The developed HER performance of H-Ni/MoO 2 can be attributed to the larger active surface area of porous hollow spherical structure and the faster electron transfer and better stability of carbon skeleton. Undoubtedly, the urea plays a crucial role to construct the hollow spherical morphology and being decomposed to form holes and amorphous carbon in the synthesized steps. The soft-template strategy using urea as the addition for forming the porous hollow structure with carbon skeleton can be extended to explore superior non-noble metal for hydrogen production. [ABSTRACT FROM AUTHOR]

[Display omitted] • NaTi 2 (PO 4) 3 /carbon is rationally designed from an all-integrated framework precursor. • Precursor is a citric acid-organic phosphonic acid skeleton chelating with Ti. • NaTi 2 (PO 4) 3 /carbon shows high capacity and superior rate capability for SIBs. • NaTi 2 (PO 4) 3 /carbon delivers an ultrastable cycling performance. Finding suitable hosts for Na+ ion storage holds the key to achieving large-scale applications of sodium-ion batteries (SIBs). NaTi 2 (PO 4) 3 is widely considered to be an advanced anode material for SIBs, because of its 3D open framework, high theoretical capacity, and good thermodynamic stability. However, the instability of electrolyte/electrode interface and intrinsic low electronic conductivity of NaTi 2 (PO 4) 3 lead to the poor cycling and rate performance. In this work, an all-integrated framework with chelating Ti in a cross-linked citric acid-organic phosphonic acid skeleton is fabricated as a precursor for the synthesis of NaTi 2 (PO 4) 3 /carbon composite. The generated interconnected carbon provides extensive support for NaTi 2 (PO 4) 3 crystal. These unique structure delivers a high reversible capacity (225.8 mAh g−1 at 0.2 A g−1), good rate performance (219.7 mAh g−1 at 0.4 A g−1, and 189.6 mAh g−1 at 1 A g−1), and superb long-term cycling stability (156.0 mAh g−1 at 2 A g−1 after 4000 cycles). It is believed that this facile and effective strategy can shed light on the development of advanced phosphate electrode materials for SIBs. [ABSTRACT FROM AUTHOR]

Phosphatidylinositol 3-Kinase (PI3K) is a key regulator of cell motility during chemotaxis and plays an important role in relaying and amplifying the shallow gradient of chemoattractant signals to ultimately mediate rearrangements of the actin cytoskeleton. To determine whether PI3K plays a similar role in electrotaxis as in chemotaxis, we examined directional cell migration in response to an electric field (EF) and unexpectedly found that the role of PI3K in regulating cell motility differs depending on the state of Dictyostelium cells. Contrary to chemotaxis experiments using aggregation-competent cells, in the cell migration assay, we used a recently developed method for electrotaxis using 3-h starved cells. Wild-type cells starved for 3 h showed increased motility in the presence of LY294002, a PI3K inhibitor, whereas aggregation-competent cells showed slightly decreased motility, indicating the effect of LY294002 on cell motility differ depending on the state of the cells. Consistent with these results, pi3k null cells in the vegetative state exhibited increased motility similar to that in the presence of LY294002 , compared to wild-type cells. These findings were confirmed through random migration experiments. These results suggest that PI3Ks play a suppressive role in regulating cell motility of vegetative Dictyostelium cells and that the suppressive effect is reversed on inhibition or lack of PI3Ks, leading to high motility. • PI3K is a key regulator of cell motility in directional cell migration. • Roles of PI3K in cell motility differ depending on the state of Dictyostelium cells. • PI3K plays an inhibitory role in regulating cell motility of vegetative cells. • Whereas, it plays a stimulatory role in cell motility of aggregation-competent cells. [ABSTRACT FROM AUTHOR]

Cell migration is essential in animal development and co-opted during metastasis and inflammatory diseases. Some cells migrate collectively, which requires them to balance epithelial characteristics such as stable cell-cell adhesions with features of motility like rapid turnover of adhesions and dynamic cytoskeletal structures. How this is regulated is not entirely clear but important to understand. While investigating Drosophila oogenesis, we found that the putative E3 ubiquitin ligase, Mind bomb 2 (Mib2), is required to promote epithelial stability and the collective cell migration of border cells. Through biochemical analysis, we identified components of Mib2 complexes, which include E-cadherin and α- and β-catenins, as well as actin regulators. We also found that three Mib2 interacting proteins, RhoGAP19D, Supervillin, and Myosin heavy chain-like, affect border cell migration. mib2 mutant main body follicle cells have drastically reduced E-cadherin-based adhesion complexes and diminished actin filaments. We conclude that Mib2 acts to stabilize E-cadherin-based adhesion complexes and promote a robust actin cytoskeletal network, which is important for maintenance of epithelial integrity. The interaction with cadherin adhesion complexes and other cytoskeletal regulators contribute to its role in collective cell migration. Since Mib2 is well conserved, it may have similar functional significance in other organisms. [Display omitted] • Drosophila Mind bomb 2, an E3 ligase, is highly expressed in ovarian follicle cells. • mind bomb 2 is required for border cell migration and epithelial character. • Mind bomb 2 interactors, RhoGAP19D, Myosin heavy chain-like , and Supervillin , act in migration. • Loss of mind bomb 2 results in reduced adhesion complexes and F-actin. Summary statement: Mind bomb 2, an E3 ubiquitin ligase, enables collective cell migration in Drosophila and promotes epithelial character by stabilizing adhesion complexes and cytoskeletal proteins. [ABSTRACT FROM AUTHOR]

Sea urchin larvae spend weeks to months feeding on plankton prior to metamorphosis. When handled in the laboratory they are easily injured, suggesting that in the plankton they are injured with some frequency. Fortunately, larval wounds are repaired through an efficient wound response with mesenchymal pigment cells and blastocoelar cells assisting as the epithelium closes. An injury to the epithelium leads to an immediate calcium transient that rapidly spreads around the entire larva and is necessary for activating pigment cell migration toward the wound. If calcium transport is blocked, the pigment cells fail to activate and remain in place. When activated, pigment cells initiate directed migration to the wound site from distances of at least 85 ​μm. Upon arrival at the wound site they participate in an innate immune response. Blastocoelar cells are recruited to the injury site as well, though the calcium transient is unnecessary for activating these cells. At the wound site, blastocoelar cells participate in several functions including remodeling the skeleton if it protrudes through the epithelium. The graphic shows a skeletal rod protruding through the epithelium of the larval arm. Pigment cells and blastocoelar cells respond to provide an immune response plus skeletal remodeling functions. A Calcium transient, initiated by the wound, rapidly spreads around the entire larva to activate the pigment cell migration toward the wound. Upon arrival at the wound pigment cells (maroon) degranulate to participate in an innate immune response. Blastocoelar cells (green) are recruited to the injury site as well. These cells exit the larva, attach to, and excise the protruding skeleton thereby allowing the epithelium to close the wound. [Display omitted] • Sea urchin larval pigment and blastocoelar cells respond to assist in injury repair. • The pigment cell response is activated by a Calcium transient. • At the injury site pigment cells release echinochrome A, a bacteriocide. • Blastocoelar cells remodel the skeleton allowing the epithelium to close the wound. [ABSTRACT FROM AUTHOR]

The 3D structured Zn anode which is grown on the surface of carbon cloth/carbon nanofiber framework (CC-CNF) can reduce the nucleation overpotential of the electrode and suppress dendrites owing to the high conductivity and abundant nucleation sites of the 3D skeleton. [Display omitted] Zn-ion battery (ZIB) is a promising electrochemical energy storage device because of the high performance, safety, and economic benefits, etc. However, the formation of Zn dendrites at anodes is seriously depressed their cycling life, Coulombic efficiency, safety, and capacity. Inhibition of Zn dendrites is considered as an efficient solution to improving the performance of ZIB. Herein, we demonstrate a 3D structured Zn anode coated in carbon nanofiber framework with carbon cloth as substrate (Zn@CC-CNF), which has the abundant Zn nucleation sites and homogeneous electrical field distribution for uniform Zn deposition, low nucleation/deposition energy barrier, and the capacity of alleviating side reactions. Thus, the Zn@CC-CNF based symmetric cells is stability operated over 400 h, which is over 400% longer than that of bare Zn coated on carbon cloth (Zn@CC). The impressive performance of the Zn@CC-CNF anode also endows the assembled Zn-MnO 2 full cell with long-term cycling stability. Better yet, the intrinsic flexibility of the carbon substrate enables the fabrication of flexible Zn-MnO 2 cell with gratifying mechanical deformation tolerance, illustrating their great application potential in flexible energy storage. [ABSTRACT FROM AUTHOR]

[Display omitted] • New Discovery : Distinguished from the reported Bi-based catalyst, the new prepared BS@Cx catalyzes CO 2 to methanol with 78% max selectivity. • New Strategy : In-situ sulfur doping strategy of forming Bi(X) species and then dispersing homogeneously active sites were proved efficiently for a catalyst of e-CO 2 RR. • New Structure : Through various characterization techniques, a special Bi-S motif supported on S-doped carbon formwork was built. Carbon dioxide as raw materials chemically transformed to valuable, renewable and high-energetic carbon feedstocks, especially if driven by renewable energy, is a desirable way to mitigate the depletion of fossil fuels and allow environmentally neutral use of carbon fuels. However, it remains more exploration of electrocatalysts with high activity and superior selectivity in converting CO 2 to storable carbon-based liquid fuels, like methanol. Herein , we develop an in-situ sulfurizing strategy over the Bi-based metal-organic frameworks (Bi-BTC) and disperse stable and special Bi-S motif on subsequent S-doped carbon-framework (called BS@Cx ). Unlike the previous reports on Bi-based catalysts, as-prepared BS@Cx converted CO 2 to methanol as major product at the whole applied potentials. Benefiting from the special Bi-S motif, it brought to the dramatic selectivity change of CO 2 reduction production: dramatic decrease in HCOO− selectivity and increase in methanol selectivity. At −0.9 V vs RHE, maximum methanol faradaic efficiency (FE) and the selectivity of methanol arrived at 78.6% and 78.8%(Total- C FE was 95.5%), respectively. Some effective experiments involving of ECSA and charge transfer efficiency (Φ) certified that BS@Cx catalysts in the form of Bi-S motif exhibited higher intrinsic activity and selectivity, and overcame the energy barrier for methanol production. Coupled with PDOS of catalyst absorbed intermediates (OCHO* and CO*) and discussion of intermediates (COOH* and CH 2 O*), we bring forward a new possible pathway for catalyzing CO 2 to methanol over BS@800. Further though microkinetic analysis with experimental Tafel slopes, we provided first-order understanding on the proposed reaction mechanisms, such as the rate-determining steps (RDS) and surface coverage (θ) of major reaction intermediates, and shed light on how rate-limiting steps can give rise to different Tafel slopes. This work may occur worthy insights into crystal structure engineering to achieve efficient electrocatalysts for selective CO 2 conversion toward generation of valuable carbon-based chemicals. [ABSTRACT FROM AUTHOR]

Cellular protrusions generated by the actin cytoskeleton are central to the process of building the body of the embryo. Problems with cellular protrusions underlie human diseases and syndromes, including implantation defects and pregnancy loss, congenital birth defects, and cancer. Cells use protrusive activity together with actin-myosin contractility to create an ordered body shape of the embryo. Here, I review how actin-rich protrusions are used by two major morphological cell types, epithelial and mesenchymal cells, during collective cell migration to sculpt the mouse embryo body. Pre-gastrulation epithelial collective migration of the anterior visceral endoderm is essential for establishing the anterior-posterior body axis. Gastrulation mesenchymal collective migration of the mesoderm wings is crucial for body elongation, and somite and heart formation. Analysis of mouse mutants with disrupted cellular protrusions revealed the key role of protrusions in embryonic morphogenesis and embryo survival. Recent technical approaches have allowed examination of the mechanisms that control cell and tissue movements in vivo in the complex 3D microenvironment of living mouse embryos. Advancing our understanding of protrusion-driven morphogenesis should provide novel insights into human developmental disorders and cancer metastasis. [ABSTRACT FROM AUTHOR]

In the process of production of freshwater pearl, implanted mantle pieces undergo a series of complex physiological and biochemical processes to form pearl sac, which produce pearl. This is a very important site of occurrence due to immune-induced biomineralization, while its molecular regulatory mechanism is still unclear. Here, we use proteomics to identify differentially expressed proteins (DEPs) of the mantle and pearl sac and examine the biomineralization and immune response of the pearl sac formation process in Hyriopsis cumingii. Using iTRAQ technology and bioinformatics analysis, we obtained DEP profiles between the mantle and pearl sac. A total of 1871 proteins were identified. Of these, 74 DEPs were found between the pearl sac and outer mantle, 112 DEPs between the pearl sac and inner mantle, and 124 DEPs between the outer and inner mantles. Bioinformatics analysis revealed that the screened biomineralization-related DEPs were mainly enriched in signaling pathways associated with calcium signaling, regulation of the actin cytoskeleton and protein processing in the endoplasmic reticulum, while the immune-related DEPs were mainly enriched in the Notch, Hippo, nuclear factor kappa-B (NF-κB), and transforming growth factor-β (TGF-β) signaling pathways. In addition, the expression of six biomineralization-related and four immune-related proteins were verified at the transcriptional level using quantitative real-time PCR. Our findings contribute to furthering the understanding of the mechanisms of pearl formation and immune response, and have long-term implications for future studies on the production of high-quality freshwater pearls and development of the freshwater pearl industry. • We used comparative proteomics to analyze immune- and biomineralization-associated DEPs and analyzed the possible joint role of both in the process of pearl sac formation. • We subdivided the mantle into outer mantle and inner mantle and compared them with each other with the pearl sac. • Our data will contribute to the understanding of the molecular mechanisms involved in pearl formation and will have implications for future research on the production of freshwater pearls. [ABSTRACT FROM AUTHOR]

We previously showed the importance of TGFβ signaling in development of the mouse axial skeleton. Here, we provide the first direct evidence that TGFβ signaling is required for resegmentation of the sclerotome using chick embryos. Lipophilic fluorescent tracers, DiO and DiD, were microinjected into adjacent somites of embryos treated with or without TGFβRI inhibitors, SB431542, SB525334 or SD208, at developmental day E2.5 (HH16). Lineage tracing of labeled cells was observed over the course of 4 days until the completion of resegmentation at E6.5 (HH32). Vertebrae were malformed and intervertebral discs were small and misshapen in inhibitor injected embryos. Hypaxial myofibers were also increased in thickness after treatment with the inhibitor. Inhibition of TGFβ signaling resulted in alterations in resegmentation that ranged between full, partial, and slanted shifts in distribution of DiO or DiD labeled cells within vertebrae. Patterning of rostro-caudal markers within sclerotome was disrupted at E3.5 after treatment with TGFβRI inhibitor with rostral domains expressing both rostral and caudal markers. We propose that TGFβ signaling regulates rostro-caudal polarity and subsequent resegmentation in sclerotome during spinal column development. [Display omitted] • Injection of TGFBR1 inhibitor in chick somites resulted in defects in axial skeleton. • TGFβ signaling was required for normal resegmentation of sclerotome. • Inhibition of TGFβ signaling resulted in altered sclerotome polarity. • Lineage tracer dyes and drug inhibitors can be used to study somite development in chick. [ABSTRACT FROM AUTHOR]

The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane compartmentalization likely candidates regulating their formation and maintenance. Indeed, recent studies suggest polarity proteins help form and maintain dendritic spines by compartmentalizing the spine neck and head. Here, we review emerging evidence that polarity proteins regulate dendritic spine plasticity and stability through the cytoskeleton, scaffolding molecules, and signaling molecules. We specifically analyze various polarity complexes known to contribute to different forms of cell polarization processes and examine the essential conceptual context linking these groups of polarity proteins to dendritic spine morphogenesis, plasticity, and cognitive functions. The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane compartmentalization likely candidates regulating their formation and maintenance. Here, we review emerging evidence that polarity proteins regulate dendritic spine plasticity and stability through the cytoskeleton, scaffolding molecules, and signaling molecules. [Display omitted] • Polarity proteins regulate the compartmentalization of dendritic spines. • Many polarity proteins regulate synaptic and cognitive functions. • Neurodevelopmental disorders have been linked to polarity proteins. [ABSTRACT FROM AUTHOR]

Microtubules are components of the cytoskeleton that perform essential functions in eukaryotes, such as those related to shape change, motility and cell division. In this context some characteristics of these filaments are essential, such as polarity and dynamic instability. In trypanosomatids, microtubules are integral to ultrastructure organization, intracellular transport and mitotic processes. Some species of trypanosomatids co-evolve with a symbiotic bacterium in a mutualistic association that is marked by extensive metabolic exchanges and a coordinated division of the symbiont with other cellular structures, such as the nucleus and the kinetoplast. It is already established that the bacterium division is microtubule-dependent, so in this work, it was investigated whether the dynamism and remodeling of these filaments is capable of affecting the prokaryote division. To this purpose, Angomonas deanei was treated with Trichostatin A (TSA), a deacetylase inhibitor, and mutant cells for histone deacetylase 6 (HDAC6) were obtained by CRISPR-Cas9. A decrease in proliferation, an enhancement in tubulin acetylation, as well as morphological and ultrastructural changes, were observed in TSA-treated protozoa and mutant cells. In both cases, symbiont filamentation occurred, indicating that prokaryote cell division is dependent on microtubule dynamism. • Proliferation reduction was reported in both TSA-treated and HDAC6 mutant cells. • Tubulin acetylation was higher in HDAC6 mutants and TSA-treated cells. • HDAC6 mutants and TSA-treated cells showed changes in the cytoskeletal arrangement. • Bacterium cytokinesis depends on microtubule acetylation levels. • HDAC6 activity is essential to the dynamic instability of microtubules in A. deanei. [ABSTRACT FROM AUTHOR]

[Display omitted] • Five pairs of novel merosesquiterpenoid enantiomers were isolated and identified. • Dauresorcinol A (1) possesses an unprecedented methyl-shifted merosesquiterpenoid carbon skeleton. • Dauresorcinol B (2) bears a novel caged merosesquiterpenoid carbon skeleton. • (+)/(−)- 1 and 3 − 5 showed more potent α -glucosidase inhibitory activity than acarbose. • The structure−activity relationships of isolates were discussed. Five pairs of new merosesquiterpenoid enantiomers, named dauresorcinols A−E (1 − 5), were isolated from the leaves of Rhododendron dauricum. Their structures were elucidated by comprehensive spectroscopic data analysis, quantum chemical calculations, Rh 2 (OCOCF 3) 4 -induced ECD, and single-crystal X-ray diffraction analysis. Dauresorcinols A (1) and B (2) possess two new merosesquiterpene skeletons bearing an unprecedented 2,6,7,10,14-pentamethyl-11-oxatetracyclo[8.8.0.02,7.012,17]octadecane and a caged 15-isohexyl-1,5,15-trimethyl-2,10-dioxatetracyclo[7.4.1.111,14.03,8]pentadecane motif, respectively. Plausible biosynthetic pathways of 1 − 5 are proposed involving key oxa-electrocyclization and Wagner−Meerwein rearrangement reactions. (+)/(−)- 1 and 3 − 5 showed potent α -glucosidase inhibitory activity, 3 to 22 times stronger than acarbose, an antidiabetic drug targeting α -glucosidase. Docking results provide a basis to design and develop merosesquiterpenoids as potent α -glycosidase inhibitors. [ABSTRACT FROM AUTHOR]

C-type lectins (CTLs) execute critical functions in multiple immune responses of crustaceans as a member of pattern recognition receptors (PRRs) family. In this study, a novel CTL was identified from the exoskeleton of the oriental river prawn Macrobrachium nipponense (Mn Lec3). The full-length cDNA of Mn Lec3 was 1150 bp with an open reading frame of 723 bp, encoding 240 amino acids. Mn Lec3 protein contained a signal peptide and one single carbohydrate-recognition domain (CRD). Mn Lec3 transcripts were widely distributed at the exoskeleton all over the body. Significant up-regulation of Mn Lec3 in exoskeleton after Aeromonas hydrophila challenged suggested the involvement of Mn Lec3 as well as the possible function of the exoskeleton in immune response. In vitro tests with recombinant Mn Lec3 protein (r Mn Lec3) manifested that it had polysaccharide binding activity, a wide spectrum of bacterial binding activity and agglutination activity only for tested Gram-negative bacteria (Escherichia coli , Vibrio anguillarum and A. hydrophila). Moreover, r Mn Lec3 significantly promoted phagocytic ability of hemocytes against A. hydrophila in vivo. What's more, Mn Lec3 interference remarkably impaired the survivability of the prawns when infected with A. hydrophila. Collectively, these results ascertained that Mn Lec3 derived from exoskeleton took an essential part in immune defense of the prawns against invading bacteria as a PRR. • A novel CTL (Mn Lec3) was identified from the exoskeleton of the oriental river prawn Macrobrachium nipponense. • Mn Lec3 plays a vital role in the immune response of the prawn. • 3.The exoskeleton might be more active in the immune response of the prawn by generating immunologic factors. [ABSTRACT FROM AUTHOR]

Filopodia are thin, actin-rich projection from the plasma membrane that promote cancer cell invasion and migration. Sex-determining region Y-related high-mobility group-box 4 (SOX4) is a crucial transcription factor that plays a role in the development and metastasis of colorectal cancer (CRC). However, the involvement of SOX4 in cytoskeleton remodeling in CRC remains unknown. For the first time, we demonstrate that SOX4 is a potent regulator of filopodia formation in CRC cells. Overexpression of SOX4 protein enhances both migration and invasion ability of HCT116, and CACO2 cells, which is relevant to the metastasis. Furthermore, through phalloidin staining, cytoskeleton re-assembly was observed in SOX4-modified cell lines. Enhanced expression of SOX4 increased the number and length of filopodia on cell surface. In contrast, silencing SOX4 in SW620 cells with higher endogenous expression of SOX4, impeded the filopodia formation. Moreover, SOX4 was found to be positively regulating the expression of central regulators of actin cytoskeleton - N -Wiskott-Aldrich syndrome protein (N -WASP); WAVE2; Actin related proteins, ARP2 and ARP3. Inhibiting the N -WASP/ARP2/3 pathway diminishes the filopodia formation and the migration of CRC cells. These results indicate the crucial role of SOX4 in the regulation of filopodia formation mediated by N -WASP/ARP2/3 pathway in CRC cells. [Display omitted] • Enhanced SOX4 expression boosts CRC cell migration and invasion via cytoskeleton remodeling. • SOX4 overexpression increases filopodia in HCT116 and CACO2 whereas silencing SOX4 reduces filopodia formation in SW620. • SOX4 mediates cytoskeleton rearrangement and migration/invasion through N -WASP/ARP2/3 pathway. [ABSTRACT FROM AUTHOR]