MALAT-1, a long non-coding RNA, is associated with metastasis, but its role in the metastatic process remains unknown. Here, we show that short-interfering RNA-mediated MALAT-1 silencing impaired cell motility of lung cancer cells and influenced the expression of numerous genes. In these genes, knockdown of any one of , , , or clearly inhibited cell migration. In MALAT-1 knockdown cells, pre-mRNA levels were decreased in some but not all genes. Thus, our findings suggest that MALAT-1 is a novel class of non-coding RNA that promotes cell motility through transcriptional and post-transcriptional regulation of motility related gene expression.
Visualizing mitochondrial fusion in real time, we identified two classes of fusion events in mammalian cells. In addition to complete fusion, we observed transient fusion events, wherein two mitochondria came into close apposition, exchanged soluble inter‐membrane space and matrix proteins, and re‐separated, preserving the original morphology. Transient fusion exhibited rapid kinetics of the sequential and separable mergers of the outer and inner membranes, but allowed only partial exchange of integral membrane proteins. When the inner membrane fusion protein Opa1 level was lowered or was greatly elevated, transient fusions could occur, whereas complete fusions disappeared. Furthermore, transient fusions began from oblique or lateral interactions of mitochondria associated with separate microtubules, whereas complete fusions resulted from longitudinal merging of organelles travelling along a single microtubule. In contrast to complete fusion, transient fusions both required and promoted mitochondrial motility. Transient fusions were also necessary and sufficient to support mitochondrial metabolism. Thus, Opa1 expression and cytoskeletal anchorage govern a novel form of fusion that has a distinct function in mitochondrial maintenance.
Hygroinduced motion is a fundamental process of energy conversion that is essential for applications that require contactless actuation in response to the day-night rhythm of atmospheric humidity. Here we demonstrate that mechanical bistability caused by rapid and anisotropic adsorption and desorption of water vapour by a flexible dynamic element that harnesses the chemical potential across very small humidity gradients for perpetual motion can be effectively modulated with light. A mechanically robust material capable of rapid exchange of water with the surroundings is prepared that undergoes swift locomotion in effect to periodic shape reconfiguration with turnover frequency of <150 min(-1). The element can lift objects similar to 85 times heavier and can transport cargos similar to 20 times heavier than itself. Having an azobenzene-containing conjugate as a photoactive dopant, this entirely humidity-driven self-actuation can be controlled remotely with ultraviolet light, thus setting a platform for next-generation smart biomimetic hybrids.
Twitching motility is a mode of solid surface translocation that occurs under humid conditions on semisolid or solid surfaces, is dependent on the presence of retractile type IV pili and is independent of the presence of a flagellum. Surface translocation via twitching motility is powered by the extension and retraction of type IV pili and can manifest as a complex multicellular collective behavior that mediates the active expansion of colonies cultured on the surface of solidified nutrient media, and of interstitial colonies that are cultured at the interface between solidified nutrient media and an abiotic material such as the base of a petri dish or a glass coverslip. Here we describe two methods for assaying twitching motility mediated interstitial colony expansion in P. aeruginosa. The first method, the "Macroscopic Twitching Assay," can be used to determine if a strain is capable of twitching motility mediated interstitial colony expansion and can also be used to quantitatively assess the influence of mutation or environmental signals on this process. The second method, the "Microscopic Twitching Assay," can be used for detailed interrogation of the movements of individual cells or small groups of bacteria during twitching motility mediated colony expansion.
Gastrointestinal motility results from coordinated contractions of the tunica muscularis, the muscular layers of the alimentary canal. Throughout most of the gastrointestinal tract, smooth muscles are organized into two layers of circularly or longitudinally oriented muscle bundles. Smooth muscle cells form electrical and mechanical junctions between cells that facilitate coordination of contractions. Excitation-contraction coupling occurs by Ca2+ entry via ion channels in the plasma membrane, leading to a rise in intracellular Ca2+. Ca2+ binding to calmodulin activates myosin light chain kinase; subsequent phosphorylation of myosin initiates cross-bridge cycling. Myosin phosphatase dephosphorylates myosin to relax muscles, and a process known as Ca2+ sensitization regulates the activity of the phosphatase. Gastrointestinal smooth muscles are 'autonomous' and generate spontaneous electrical activity (slow waves) that does not depend upon input from nerves. Intrinsic pacemaker activity comes from interstitial cells of Cajal, which are electrically coupled to smooth muscle cells. Patterns of contractile activity in gastrointestinal muscles are determined by inputs from enteric motor neurons that innervate smooth muscle cells and interstitial cells. Here we provide an overview of the cells and mechanisms that generate smooth muscle contractile behaviour and gastrointestinal motility.
Hepatocyte growth factor/scatter factor and its receptor, the tyrosine kinase Met, arose late in evolution and are unique to vertebrates. In spite of this, Met uses molecules such as Gab1 - homologues of which are present in Caenorhabditis elegans and Drosophila melanogaster for downstream signalling. Pivotal roles for Met in development and cancer have been established: Met controls cell migration and growth in embryogenesis; it also controls growth, invasion and metastasis in cancer cells; and activating Met mutations predispose to human cancer.