Concert recording 2017-12-05a

[Track 1]. Lou Brouwer medley / Brouwer -- [Track 2]. One summer\u27s day / Daniel Asbun -- [Track 3]. What a friend we have in Jesus / Brad Paisley -- [Track 4]. Unity village / Pat Metheny -- [Track 5] Truth? / Asher Perkins -- [Track 6]. Invention no. 13 / J.S. Bach -- [Track 7]. Black Orpheus / Stan Getz arranged Luiz Bonfa -- [Track 8]. Five Hawaiian minutes / Shiro Mori -- [Track 9]. Birks works / Dizzy Gillespie -- [Track 10]. Perhaps / Charlie Parker -- [Track 11]. The river / King Gizzard and the Lizard Wizard -- [Track 12]. Minor swing / Django Reinhardt and Stephan Grappelli -- [Track 13]. Why break mine / Legally blind -- [Track 14]. Monochrome / Carlie Spiers -- [Track 15]. Stuck in voodoo / Dawson Scantling -- [Track 16]. I\u27m saved / Shelby Sprott -- [Track 17]. Newborn / Muse -- [Track 18]. Blueberry brain / Elephantom

Membrane tension controls adhesion positioning at the leading edge of cells

Cell migration is dependent on adhesion dynamics and actin cytoskeleton remodeling at the leading edge. These events may be physically constrained by the plasma membrane. Here, we show that the mechanical signal produced by an increase in plasma membrane tension triggers the positioning of new rows of adhesions at the leading edge. During protrusion, as membrane tension increases, velocity slows, and the lamellipodium buckles upward in a myosin II-independent manner. The buckling occurs between the front of the lamellipodium, where nascent adhesions are positioned in rows, and the base of the lamellipodium, where a vinculin-dependent clutch couples actin to previously positioned adhesions. As membrane tension decreases, protrusion resumes and buckling disappears, until the next cycle. We propose that the mechanical signal of membrane tension exerts upstream control in mechanotransduction by periodically compressing and relaxing the lamellipodium, leading to the positioning of adhesions at the leading edge of cells

Persistent and polarised global actin flow is essential for directionality during cell migration

Cell migration is hypothesized to involve a cycle of behaviours beginning with leading edge extension. However, recent evidence suggests that the leading edge may be dispensable for migration, raising the question of what actually controls cell directionality. Here, we exploit the embryonic migration of Drosophila macrophages to bridge the different temporal scales of the behaviours controlling motility. This approach reveals that edge fluctuations during random motility are not persistent and are weakly correlated with motion. In contrast, flow of the actin network behind the leading edge is highly persistent. Quantification of actin flow structure during migration reveals a stable organization and asymmetry in the cell-wide flowfield that strongly correlates with cell directionality. This organization is regulated by a gradient of actin network compression and destruction, which is controlled by myosin contraction and cofilin-mediated disassembly. It is this stable actin-flow polarity, which integrates rapid fluctuations of the leading edge, that controls inherent cellular persistence