Many cell movements proceed via a crawling mechanism, where polymerization of the cytoskeletal protein actin pushes out the leading edge membrane. In this model, membrane tension has been seen as an impediment to filament growth and cell motility. Here we use a simple model of cell motility, the Caenorhabditis elegans sperm cell, to test how membrane tension affects movement and cytoskeleton dynamics. To enable these analyses, we create transgenic worm strains carrying sperm with a fluorescently labeled cytoskeleton. Via osmotic shock and deoxycholate treatments, we relax or tense the cell membrane and quantify apparent membrane tension changes by the membrane tether technique. Surprisingly, we find that membrane tension reduction is correlated with a decrease in cell displacement speed, whereas an increase in membrane tension enhances motility. We further demonstrate that apparent polymerization rates follow the same trends. We observe that membrane tension reduction leads to an unorganized, rough lamellipodium, composed of short filaments angled away from the direction of movement. On the other hand, an increase in tension reduces lateral membrane protrusions in the lamellipodium, and filaments are longer and more oriented toward the direction of movement. Overall we propose that membrane tension optimizes motility by streamlining polymerization in the direction of movement, thus adding a layer of complexity to our current understanding of how membrane tension enters into the motility equation. I n crawling cells, motility is mainly driven by actin polymerization, which forms filaments beneath the leading edge cell membrane to make protrusions (1). In this scenario, polymerization is inhibited by the presence of the cell membrane, and membrane tension is thus commonly seen as an impediment to cell motility (2). Experiments show that lamellipodial extension rate is indeed inversely correlated with membrane tension (3), but steady-state, whole cell translocation has not been studied. Here we use a simplified system of crawling cell motility, the Caenorhabditis elegans sperm cell, in order to address the question of how membrane tension affects whole cell translocation. The sperm cell contains only cytoskeleton, mitochondria, and nuclear material and is incapable of de novo protein synthesis or classical exo-and endocytosis, thus representing a useful model for exploring the interplay between membrane tension and cell motility. The sperm cell translocates by adhering to the substrate and emitting a dynamic lamellipodia, in a manner that is morphologically similar to actomyosin containing motile cells, despite the fact that the movement of sperm cells is powered by the dynamics of the major sperm protein (MSP) cytoskeleton in the absence of actin and known molecular motors (4, 5).The production of fluorescently labeled actin in living cells was a watershed in the understanding of how actin structures assemble, flow, and disassemble to produce cell motility. However, due to efficient gene silencing mechanisms in th...
Furrow ingression in animal cell cytokinesis is controlled by phosphorylation of myosin II regulatory light chain (mRLC). In Caenorhabditis elegans embryos, Rho-dependent Kinase (RhoK) is involved in, but not absolutely required for, this phosphorylation. The calmodulin effector myosin light chain kinase (MLCK) can also phosphorylate mRLC and is widely regarded as a candidate for redundant function with RhoK. However, our results show that RNA mediated interference against C. elegans calmodulin and candidate MLCKs had no effect on cytokinesis in wild-type or RhoK mutant embryos, ruling out the calmodulin/MLCK pathway as the missing regulator of cytokinesis in the C. elegans early embryo.
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