Levitation and controlled motion of matter in air have a wealth of potential applications ranging from materials processing to biochemistry and pharmaceuticals. We present a unique acoustophoretic concept for the contactless transport and handling of matter in air. Spatiotemporal modulation of the levitation acoustic field allows continuous planar transport and processing of multiple objects, from near-spherical (volume of 0.1-10 μL) to wire-like, without being limited by the acoustic wavelength. The independence of the handling principle from special material properties (magnetic, optical, or electrical) is illustrated with a wide palette of application experiments, such as contactless droplet coalescence and mixing, solid-liquid encapsulation, absorption, dissolution, and DNA transfection. More than a century after the pioneering work of Lord Rayleigh on acoustic radiation pressure, a path-breaking concept is proposed to harvest the significant benefits of acoustic levitation in air.acoustics | fluid | ultrasounds | manipulation | microfluidics
IQGAP1 is a conserved modular protein overexpressed in cancer and involved in organizing actin and microtubules in motile processes such as adhesion, migration, and cytokinesis. A variety of proteins have been shown to interact with IQGAP1, including the small G proteins Rac1 and Cdc42, actin, calmodulin, -catenin, the microtubule plus end-binding proteins CLIP170 (cytoplasmic linker protein) and adenomatous polyposis coli. However, the molecular mechanism by which IQGAP1 controls actin dynamics in cell motility is not understood. Quantitative co-localization analysis and down-regulation of IQGAP1 revealed that IQGAP1 controls the co-localization of N-WASP with the Arp2/3 complex in lamellipodia. Co-immunoprecipitation supports an in vivo link between IQGAP1 and N-WASP. Pull-down experiments and kinetic assays of branched actin polymerization with N-WASP and Arp2/3 complex demonstrated that the C-terminal half of IQGAP1 activates N-WASP by interacting with its BR-CRIB domain in a Cdc42-like manner, whereas the N-terminal half of IQGAP1 antagonizes this activation by association with a C-terminal region of IQGAP1. We propose that signal-induced relief of the autoinhibited fold of IQGAP1 allows activation of N-WASP to stimulate Arp2/3-dependent actin assembly.Directional cell migration results from the coordination of protrusion formation and cell adhesion. Although the concerted re-organization of actin and microtubules establishes and maintains cell polarization during directional movement, little is known about the molecular mechanisms underlying signal-mediated crosstalk between the two different cytoskeletal arrays (1). In this context, the modular IQGAP1 protein has received intense interest in the past years (2). The multiple partners of IQGAP1, including signaling molecules like Cdc42 or Rac1, calmodulin (3-6), and adhesion/cytoskeletal proteins like -catenin, E-cadherin, actin filaments, and microtubule plus end-tracking proteins (CLIP170 and adenomatous polyposis coli (APC)) strongly suggest that IQGAP1 is an important player in coordinating cell polarity, adhesion, and migration (7-13). Concrete support to this view was brought by evidence showing that IQGAP1 is overexpressed in cancer (14, 15), controls cytokinesis (16 -21), and cell-cell adhesion (22-24). In addition, recent reports showed that IQGAP1 localizes in lamellipodia of motile cells (4,25,26) where it may link microtubule ends to the actin cytoskeleton (12,27) and that overexpression of IQGAP1 increases cell motility, whereas knockdown of the protein reduces cell migration and inhibits the formation of a protrusive actin meshwork at the leading edge (25). Finally, IQGAP1 regulates E-cadherinmediated cell-cell adhesion both positively and negatively (11). However, the functional and molecular link between IQGAP1 and the actin cytoskeleton in cell-cell adhesions and in lamellipodia has remained elusive.Extension of lamellipodia is driven by stimulus-responsive WASP family proteins (N-WASP, WASP, and Scar/WAVE) Cortactin and CARMIL, which act...
The time required to re-establish a functioning endothelial cell layer after vascular implant placement is critical to the success of the respective cardiologic or surgical intervention. Topographic modifications of implant surfaces promise to expedite endothelial regeneration by triggering the activation of cellular machineries that facilitate cell spreading. Exploiting nanoimprint lithography techniques on cyclic olefin copolymer foils, we engineered biocompatible submicron-and micro-structured gratings with groove and ridge width of 1 or 5 mm and groove depth ranging from 0.1 to 2 mm. Our results reveal that both the onset of endothelial spreading and subsequent texture-guided cell polarization critically depend on the feature size of the underlying topography, yet are independently modulated by the surface texture. Specifically, we demonstrate that on gratings with ridge and groove width of 1 mm and groove depth of 1 mm or deeper, the onset of endothelial spreading is 40% faster than on flat substrates, and that the cells align within ten degrees to the gratings. On this topography, we identify two independently regulated phases: acceleration of the onset of spreading supported by the rapid activation of integrin signaling proceeding via Focal Adhesion Kinase, and contact guidance which requires ROCK1/2 and myosin-II dependent cell contractility and focal adhesion maturation.
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