Статті в журналах: "Crawling motility"

1

Recho, Pierre, Thibaut Putelat, and Lev Truskinovsky. "Mechanics of motility initiation and motility arrest in crawling cells." Journal of the Mechanics and Physics of Solids 84 (November 2015): 469–505. http://dx.doi.org/10.1016/j.jmps.2015.08.006.

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2

Yamasaki, Akira, Michiyo Suzuki, Tomoo Funayama, Takahito Moriwaki, Tetsuya Sakashita, Yasuhiko Kobayashi, and Qiu-Mei Zhang-Akiyama. "High-Dose Irradiation Inhibits Motility and Induces Autophagy in Caenorhabditis elegans." International Journal of Molecular Sciences 22, no. 18 (September 10, 2021): 9810. http://dx.doi.org/10.3390/ijms22189810.

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Radiation damages many cellular components and disrupts cellular functions, and was previously reported to impair locomotion in the model organism Caenorhabditis elegans. However, the response to even higher doses is not clear. First, to investigate the effects of high-dose radiation on the locomotion of C. elegans, we investigated the dose range that reduces whole-body locomotion or leads to death. Irradiation was performed in the range of 0–6 kGy. In the crawling analysis, motility decreased after irradiation in a dose-dependent manner. Exposure to 6 kGy of radiation affected crawling on agar immediately and caused the complete loss of motility. Both γ-rays and carbon-ion beams significantly reduced crawling motility at 3 kGy. Next, swimming in buffer was measured as a motility index to assess the response over time after irradiation and motility similarly decreased. However, swimming partially recovered 6 h after irradiation with 3 kGy of γ-rays. To examine the possibility of a recovery mechanism, in situ GFP reporter assay of the autophagy-related gene lgg-1 was performed. The fluorescence intensity was stronger in the anterior half of the body 7 h after irradiation with 3 kGy of γ-rays. GFP::LGG-1 induction was observed in the pharynx, neurons along the body, and the intestine. Furthermore, worms were exposed to region-specific radiation with carbon-ion microbeams and the trajectory of crawling was measured by image processing. Motility was lower after anterior-half body irradiation than after posterior-half body irradiation. This further supported that the anterior half of the body is important in the locomotory response to radiation.

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3

Alteraifi, A. M., and D. V. Zhelev. "Transient increase of free cytosolic calcium during neutrophil motility responses." Journal of Cell Science 110, no. 16 (August 15, 1997): 1967–77. http://dx.doi.org/10.1242/jcs.110.16.1967.

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The release of free cytosolic calcium is a secondary messenger for many cell functions. Here we study the coupling between the release of intracellular calcium and motility responses of the human neutrophil. Two groups of motility responses are studied: motility responses in the presence of adhesion, such as cell crawling and phagocytosis, and motility responses ‘in suspension’, such as pseudopod formation. The motility responses are stimulated by the chemoattractant N-formyl-methionyl-leucyl-phenylalanine (fMLP) and the release of calcium is monitored by measuring the fluorescence from fluo-3. fMLP induces a single release of free cytosolic calcium both in suspended cells and in crawling cells. Calcium release is a threshold process where the number of cells releasing calcium is dependent on the chemoattractant concentration while the amount of released calcium is not. For suspended cells the threshold fMLP concentration for calcium release is in the order of 10(−7) M, while for crawling cells it is in the order of 5x10(−9) M. The smaller value of the threshold fMLP concentration for crawling cells compared to that for suspended cells suggests that bound adhesion receptors are involved in the calcium release. The threshold fMLP concentration for suspended cells is also larger than the minimum fMLP concentration (in the order of 10(−10) M) for initiating pseudopod formation. So, there is a range of fMLP concentrations where pseudopod formation occurs without calcium release. To explore this relationship further, pseudopod extension and calcium release are stimulated many times in a single cell by using fMLP concentrations above the threshold. The result is that calcium release is desensitized by fMLP while pseudopod extension is not. All the results taken together suggest that the release of free cytosolic calcium and the rearrangement of the F-actin network during motility follow different signaling pathways.

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4

Mai, Melissa H., and Brian A. Camley. "Hydrodynamic effects on the motility of crawling eukaryotic cells." Soft Matter 16, no. 5 (2020): 1349–58. http://dx.doi.org/10.1039/c9sm01797f.

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5

Bottino, Dean, Alexander Mogilner, Tom Roberts, Murray Stewart, and George Oster. "How nematode sperm crawl." Journal of Cell Science 115, no. 2 (January 15, 2002): 367–84. http://dx.doi.org/10.1242/jcs.115.2.367.

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Sperm of the nematode, Ascaris suum, crawl using lamellipodial protrusion, adhesion and retraction, a process analogous to the amoeboid motility of other eukaryotic cells. However, rather than employing an actin cytoskeleton to generate locomotion, nematode sperm use the major sperm protein (MSP). Moreover, nematode sperm lack detectable molecular motors or the battery of actin-binding proteins that characterize actin-based motility. The Ascaris system provides a simple ‘stripped down’ version of a crawling cell in which to examine the basic mechanism of cell locomotion independently of other cellular functions that involve the cytoskeleton. Here we present a mechanochemical analysis of crawling in Ascaris sperm. We construct a finite element model wherein (a) localized filament polymerization and bundling generate the force for lamellipodial extension and (b) energy stored in the gel formed from the filament bundles at the leading edge is subsequently used to produce the contraction that pulls the rear of the cell forward. The model reproduces the major features of crawling sperm and provides a framework in which amoeboid cell motility can be analyzed. Although the model refers primarily to the locomotion of nematode sperm, it has important implications for the mechanics of actin-based cell motility.Movies available on-line.

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6

Boscacci, Rémy T., Friederike Pfeiffer, Kathrin Gollmer, Ana Isabel Checa Sevilla, Ana Maria Martin, Silvia Fernandez Soriano, Daniela Natale, et al. "Comprehensive analysis of lymph node stroma-expressed Ig superfamily members reveals redundant and nonredundant roles for ICAM-1, ICAM-2, and VCAM-1 in lymphocyte homing." Blood 116, no. 6 (August 12, 2010): 915–25. http://dx.doi.org/10.1182/blood-2009-11-254334.

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Abstract Although it is well established that stromal intercellular adhesion molecule-1 (ICAM-1), ICAM-2, and vascular cell adhesion molecule-1 (VCAM-1) mediate lymphocyte recruitment into peripheral lymph nodes (PLNs), their precise contributions to the individual steps of the lymphocyte homing cascade are not known. Here, we provide in vivo evidence for a selective function for ICAM-1 > ICAM-2 > VCAM-1 in lymphocyte arrest within noninflamed PLN microvessels. Blocking all 3 CAMs completely inhibited lymphocyte adhesion within PLN high endothelial venules (HEVs). Postarrest extravasation of T cells was a 3-step process, with optional ICAM-1–dependent intraluminal crawling followed by rapid ICAM-1– or ICAM-2–independent diapedesis and perivascular trapping. Parenchymal motility of lymphocytes was modestly reduced in the absence of ICAM-1, while ICAM-2 and α4-integrin ligands were not required for B-cell motility within follicles. Our findings highlight nonredundant functions for stromal Ig family CAMs in shear-resistant lymphocyte adhesion in steady-state HEVs, a unique role for ICAM-1 in intraluminal lymphocyte crawling but redundant roles for ICAM-1 and ICAM-2 in lymphocyte diapedesis and interstitial motility.

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7

Paoletti, P., and L. Mahadevan. "A proprioceptive neuromechanical theory of crawling." Proceedings of the Royal Society B: Biological Sciences 281, no. 1790 (September 7, 2014): 20141092. http://dx.doi.org/10.1098/rspb.2014.1092.

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The locomotion of many soft-bodied animals is driven by the propagation of rhythmic waves of contraction and extension along the body. These waves are classically attributed to globally synchronized periodic patterns in the nervous system embodied in a central pattern generator (CPG). However, in many primitive organisms such as earthworms and insect larvae, the evidence for a CPG is weak, or even non-existent. We propose a neuromechanical model for rhythmically coordinated crawling that obviates the need for a CPG, by locally coupling the local neuro-muscular dynamics in the body to the mechanics of the body as it interacts frictionally with the substrate. We analyse our model using a combination of analytical and numerical methods to determine the parameter regimes where coordinated crawling is possible and compare our results with experimental data. Our theory naturally suggests mechanisms for how these movements might arise in developing organisms and how they are maintained in adults, and also suggests a robust design principle for engineered motility in soft systems.

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8

Mai, Melissa H., and Brian A. Camley. "Transition between Swimming and Crawling: A Model of Eukaryotic Cell Motility." Biophysical Journal 116, no. 3 (February 2019): 546a. http://dx.doi.org/10.1016/j.bpj.2018.11.2938.

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9

Ehrengruber, M. U., D. A. Deranleau, and T. D. Coates. "Shape oscillations of human neutrophil leukocytes: characterization and relationship to cell motility." Journal of Experimental Biology 199, no. 4 (April 1, 1996): 741–47. http://dx.doi.org/10.1242/jeb.199.4.741.

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When neutrophil leukocytes are stimulated by chemotactic factors or by substratum contact, they change their shape. Shape changes are a prerequisite for cellular migration and typically involve the extrusion of thin, veil-like lamellipods and the development of morphological polarity. Stimulation also leads to changes in the neutrophil content of filamentous actin (F-actin), which is the major cytoskeletal component. Suspensions of human neutrophils stimulated with chemoattractants exhibit sinusoidal light-scattering oscillations with a period of approximately 8 s at 37 degrees C. These oscillations arise from periodic fluctuations in the cell body size caused by lamellipod extension and retraction cycles. The light-scattering oscillations are paralleled by corresponding oscillations in F-actin content. This raises the interesting possibility that cyclic actin polymerization constitutes the driving force for shape oscillations of suspended neutrophils. Similar periodic shape changes are present in neutrophils crawling on a surface, suggesting that shape oscillations are important for neutrophil motion. This review summarizes our present knowledge about shape oscillations in suspended and crawling neutrophils and discusses a possible role for these oscillations in neutrophil motility.

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10

Nakamura, Shuichi. "Motility of the Zoonotic Spirochete Leptospira: Insight into Association with Pathogenicity." International Journal of Molecular Sciences 23, no. 3 (February 7, 2022): 1859. http://dx.doi.org/10.3390/ijms23031859.

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If a bacterium has motility, it will use the ability to survive and thrive. For many pathogenic species, their motilities are a crucial virulence factor. The form of motility varies among the species. Some use flagella for swimming in liquid, and others use the cell-surface machinery to move over solid surfaces. Spirochetes are distinguished from other bacterial species by their helical or flat wave morphology and periplasmic flagella (PFs). It is believed that the rotation of PFs beneath the outer membrane causes transformation or rolling of the cell body, propelling the spirochetes. Interestingly, some spirochetal species exhibit motility both in liquid and over surfaces, but it is not fully unveiled how the spirochete pathogenicity involves such amphibious motility. This review focuses on the causative agent of zoonosis leptospirosis and discusses the significance of their motility in liquid and on surfaces, called crawling, as a virulence factor.

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11

Tahara, Hajime, Kyosuke Takabe, Yuya Sasaki, Kie Kasuga, Akihiro Kawamoto, Nobuo Koizumi, and Shuichi Nakamura. "The mechanism of two-phase motility in the spirochete Leptospira : Swimming and crawling." Science Advances 4, no. 5 (May 2018): eaar7975. http://dx.doi.org/10.1126/sciadv.aar7975.

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12

Cucchi, Alessandro, Antoine Mellet, and Nicolas Meunier. "Self polarization and traveling wave in a model for cell crawling migration." Discrete & Continuous Dynamical Systems 42, no. 5 (2022): 2381. http://dx.doi.org/10.3934/dcds.2021194.

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<p style='text-indent:20px;'>In this paper, we prove the existence of traveling wave solutions for an incompressible Darcy's free boundary problem recently introduced in [<xref ref-type="bibr" rid="b6">6</xref>] to describe cell motility. This free boundary problem involves a nonlinear destabilizing term in the boundary condition which describes the active character of the cell cytoskeleton. By using two different methods, a constructive method via a graph analysis and a local bifurcation method, we prove that traveling wave solutions exist when the destabilizing term is strong enough.</p>

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13

DeSimone, Antonio, and Giancarlo Cicconofri. "Swimming and crawling motility at microscopic scales: from biological templates to bio-inspired devices." IFAC-PapersOnLine 48, no. 1 (2015): 825–26. http://dx.doi.org/10.1016/j.ifacol.2015.05.179.

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14

Small, J. Victor, Kurt Anderson, and Klemens Rottner. "Actin and the coordination of protrusion, attachment and retraction in cell crawling." Bioscience Reports 16, no. 5 (October 1, 1996): 351–68. http://dx.doi.org/10.1007/bf01207261.

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To crawl over a substrate a cell must first protrude in front, establish new attachments to the substrate and then retract its rear. Protrusion and retraction utilise different subcompartments of the actin cytoskeleton and operate by different mechanisms, one involving actin polymerization and the other myosin-based contraction. Using as examples the rapidly locomoting keratocyte and the slowly moving fibroblast we illustrate how over expression of one or the other actin subcompartments leads to the observed differences in motility. We also propose, that despite these differences there is a common coordination mechanism underlying the genesis of the actin cytoskeleton that involves the nucleation of actin filaments at the protruding cell front, in the lamellipodium, and the relocation of these filaments, via polymerization and flow, to the more posterior actin filament compartments.

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15

Fritz-Laylin, Lillian K., Samuel J. Lord, and R. Dyche Mullins. "WASP and SCAR are evolutionarily conserved in actin-filled pseudopod-based motility." Journal of Cell Biology 216, no. 6 (May 4, 2017): 1673–88. http://dx.doi.org/10.1083/jcb.201701074.

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Diverse eukaryotic cells crawl through complex environments using distinct modes of migration. To understand the underlying mechanisms and their evolutionary relationships, we must define each mode and identify its phenotypic and molecular markers. In this study, we focus on a widely dispersed migration mode characterized by dynamic actin-filled pseudopods that we call “α-motility.” Mining genomic data reveals a clear trend: only organisms with both WASP and SCAR/WAVE—activators of branched actin assembly—make actin-filled pseudopods. Although SCAR has been shown to drive pseudopod formation, WASP’s role in this process is controversial. We hypothesize that these genes collectively represent a genetic signature of α-motility because both are used for pseudopod formation. WASP depletion from human neutrophils confirms that both proteins are involved in explosive actin polymerization, pseudopod formation, and cell migration. WASP and WAVE also colocalize to dynamic signaling structures. Moreover, retention of WASP together with SCAR correctly predicts α-motility in disease-causing chytrid fungi, which we show crawl at >30 µm/min with actin-filled pseudopods. By focusing on one migration mode in many eukaryotes, we identify a genetic marker of pseudopod formation, the morphological feature of α-motility, providing evidence for a widely distributed mode of cell crawling with a single evolutionary origin.

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16

Rafelski, Susanne M., and Julie A. Theriot. "Crawling Toward a Unified Model of Cell Motility: Spatial and Temporal Regulation of Actin Dynamics." Annual Review of Biochemistry 73, no. 1 (June 2004): 209–39. http://dx.doi.org/10.1146/annurev.biochem.73.011303.073844.

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17

Ziebert, Falko, and Igor S. Aranson. "Effects of Adhesion Dynamics and Substrate Compliance on the Shape and Motility of Crawling Cells." PLoS ONE 8, no. 5 (May 31, 2013): e64511. http://dx.doi.org/10.1371/journal.pone.0064511.

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18

Volkov, Yuri, Aideen Long та Dermot Kelleher. "Inside the Crawling T Cell: Leukocyte Function-Associated Antigen-1 Cross-Linking Is Associated with Microtubule-Directed Translocation of Protein Kinase C Isoenzymes β(I) and δ". Journal of Immunology 161, № 12 (15 грудня 1998): 6487–95. http://dx.doi.org/10.4049/jimmunol.161.12.6487.

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Abstract T cells activated via integrin receptors can polarize and start crawling locomotion with repeated cycles of cytoskeletal reassembly processes, many of which depend on phosphorylation. We demonstrate that protein kinase C (PKC) activation represents an essential event in induction of active T cell motility. We find that in crawling T cells triggered via cross-linking of integrin LFA-1 two PKC isoenzymes, β(I) and δ, are targeted to the cytoskeleton with specific localization corresponding to the microtubule-organizing center (MTOC) and microtubules, as detected by immunocytochemistry and immunoblotting. Clustering of LFA-1 associated with its signaling function also occurs at the membrane sites adjacent to the MTOC. We further show that cells of a PKC-β-deficient clone derived from parental PKC-β-expressing T cell line can neither crawl nor develop a polarized microtubule array upon integrin cross-linking. However, their adhesion and formation of actin-based pseudopodia remain unaffected. Our data demonstrate the critical importance of the microtubule cytoskeleton in T cell locomotion and suggest a novel microtubule-directed intracellular signaling pathway mediated by integrins and involving two distinctive PKC isoforms.

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19

Zhang, Shun, Danielle Skinner, Prateek Joshi, Ernesto Criado-Hidalgo, Yi-Ting Yeh, Juan C. Lasheras, Conor R. Caffrey, and Juan C. del Alamo. "Quantifying the mechanics of locomotion of the schistosome pathogen with respect to changes in its physical environment." Journal of The Royal Society Interface 16, no. 150 (January 2019): 20180675. http://dx.doi.org/10.1098/rsif.2018.0675.

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Schistosomiasis is a chronic and morbid disease of poverty affecting approximately 200 million people worldwide. Mature schistosome flatworms wander in the host's hepatic portal and mesenteric venous system where they encounter a range of blood flow conditions and geometrical confinement. However, the mechanisms that support schistosome locomotion and underlie the pathogen's adaptation to its physical environment are largely unknown. By combining microfabrication and traction force microscopy, we developed various in vitro assays to quantify the mechanics of locomotion of adult male Schistosoma mansoni in different physiologically relevant conditions. We show that in unconfined settings, the parasite undergoes two-anchor marching mediated by the coordinated action of its oral and ventral suckers. This mode of locomotion is maintained when the worm faces an external flow, to which it responds by adjusting the strength of its suckers. In geometrically confined conditions, S. mansoni switches to a different crawling modality by generating retrograde peristaltic waves along its body, a mechanism shared with terrestrial and marine worms. However, while the surface of most worms has backward-pointing bristles that rectify peristaltic waves and facilitate forward locomotion, S. mansoni has isotropically oriented tubercles. This requires tight coordination between muscle contraction and substrate friction but gives S. mansoni the ability to reverse its direction of locomotion without turning its body, which is likely advantageous to manoeuvre in narrow-bore vessels. We show that the parasite can also coordinate the action of its suckers with its peristaltic body contractions to increase crawling speed. Throughout this study, we report on a number of biomechanical parameters to quantify the motility of adult schistosomes (e.g. sucker grabbing strength, the rate of detachment under flow, peristaltic wave properties and traction stresses). The new series of in vitro assays make it possible to quantify key phenotypical aspects of S. mansoni motility that could guide the discovery of new drugs to treat schistosomiasis.

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20

Yi, Kexi, Xu Wang, Mark R. Emmett, Alan G. Marshall, Murray Stewart, and Thomas M. Roberts. "Dephosphorylation of Major Sperm Protein (MSP) Fiber Protein 3 by Protein Phosphatase 2A during Cell Body Retraction in the MSP-based Amoeboid Motility of Ascaris Sperm." Molecular Biology of the Cell 20, no. 14 (July 15, 2009): 3200–3208. http://dx.doi.org/10.1091/mbc.e09-03-0240.

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The crawling movement of nematode sperm requires coordination of leading edge protrusion with cell body retraction, both of which are powered by modulation of a cytoskeleton based on major sperm protein (MSP) filaments. We used a cell-free in vitro motility system in which both protrusion and retraction can be reconstituted, to identify two proteins involved in cell body retraction. Pharmacological and depletion-add back assays showed that retraction was triggered by a putative protein phosphatase 2A (PP2A, a Ser/Thr phosphatase activated by tyrosine dephosphorylation). Immunofluorescence showed that PP2A was present in the cell body and was concentrated at the base of the lamellipod where the force for retraction is generated. PP2A targeted MSP fiber protein 3 (MFP3), a protein unique to nematode sperm that binds to the MSP filaments in the motility apparatus. Dephosphorylation of MFP3 caused its release from the cytoskeleton and generated filament disassembly. Our results suggest that interaction between PP2A and MFP3 leads to local disassembly of the MSP cytoskeleton at the base of the lamellipod in sperm that in turn pulls the trailing cell body forward.

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21

Sepsenwol, S., H. Ris, and T. M. Roberts. "A unique cytoskeleton associated with crawling in the amoeboid sperm of the nematode, Ascaris suum." Journal of Cell Biology 108, no. 1 (January 1, 1989): 55–66. http://dx.doi.org/10.1083/jcb.108.1.55.

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Nematode sperm extend pseudopods and pull themselves over substrates. They lack an axoneme or the actin and myosins of other types of motile cells, but their pseudopods contain abundant major sperm protein (MSP), a family of 14-kD polypeptides found exclusively in male gametes. Using high voltage electron microscopy, a unique cytoskeleton was discovered in the pseudopod of in vitro-activated, crawling sperm of the pig intestinal nematode Ascaris suum. It consists of 5-10-nm fuzzy fibers organized into 150-250-nm-thick fiber complexes, which connect to each of the moving pseudopodial membrane projections, villipodia, which in turn make contact with the substrate. Individual fibers in a complex splay out radially from its axis in all directions. The centripetal ends intercalate with fibers from other complexes or terminate in a thickened layer just beneath the pseudopod membrane. Monoclonal antibodies directed against MSP heavily label the fiber complexes as well as individual pseudopodial filaments throughout their length. This represents the first evidence that MSP may be the major filament protein in the Ascaris sperm cytoskeleton. The large fiber complexes can be seen clearly in the pseudopods of live, crawling sperm by computer-enhanced video, differential-interference contrast microscopy, forming with the villipodia at the leading edge of the sperm pseudopod. Even before the pseudopod attaches, the entire cytoskeleton and villipodia move continuously rearwards in unison toward the cell body. During crawling, complexes and villipodia in the pseudopod recede at the same speed as the spermatozoon moves forward, both disappearing at the pseudopod-cell body junction. Sections at this region of high membrane turnover reveal a band of densely packed smooth vesicles with round and tubular profiles, some of which are associated with the pseudopod plasma membrane. The exceptional anatomy, biochemistry, and phenomenology of Ascaris sperm locomotion permit direct study of the involvement of the cytoskeleton in amoeboid motility.

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22

Opas, Michal. "Cellular adhesiveness, contractility, and traction: stick, grip, and slip control." Biochemistry and Cell Biology 73, no. 7-8 (July 1, 1995): 311–16. http://dx.doi.org/10.1139/o95-039.

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Translocation of cells over solid substrata depends on generation of motive force, in crawling tissue cells, brought about by regulated contractility of intracellular actomyosin. Intracellular contractile machinery has a direct, structural connection to the cell surface. Hence, regulated adhesiveness of the cell surface provides a mechanism whereby a cell can fine tune the extent of tractional forces that are necessary for effective translocation. Cells are able to control adhesiveness of surfaces (stick), contractility (grip), and the extent of traction exerted on the substratum (slip). Here, I discuss several aspects of local (subcellular) regulation of adhesiveness and contractility and speculate on how cells, given a choice of the substratum, decide on how and where to apply traction.Key words: cell adhesion, focal contacts, cell motility, traction, cytomechanics.

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23

Buttery, Shawnna M., Gail C. Ekman, Margaret Seavy, Murray Stewart, and Thomas M. Roberts. "Dissection of the Ascaris Sperm Motility Machinery Identifies Key Proteins Involved in Major Sperm Protein-based Amoeboid Locomotion." Molecular Biology of the Cell 14, no. 12 (December 2003): 5082–88. http://dx.doi.org/10.1091/mbc.e03-04-0246.

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Although Ascaris sperm motility closely resembles that seen in many other types of crawling cells, the lamellipodial dynamics that drive movement result from modulation of a cytoskeleton based on the major sperm protein (MSP) rather than actin. The dynamics of the Ascaris sperm cytoskeleton can be studied in a cell-free in vitro system based on the movement of plasma membrane vesicles by fibers constructed from bundles of MSP filaments. In addition to ATP, MSP, and a plasma membrane protein, reconstitution of MSP motility in this cell-free extract requires cytosolic proteins that orchestrate the site-specific assembly and bundling of MSP filaments that generates locomotion. Here, we identify a fraction of cytosol that is comprised of a small number of proteins but contains all of the soluble components required to assemble fibers. We have purified two of these proteins, designated MSP fiber proteins (MFPs) 1 and 2 and demonstrated by immunolabeling that both are located in the MSP cytoskeleton in cells and in fibers. These proteins had reciprocal effects on fiber assembly in vitro: MFP1 decreased the rate of fiber growth, whereas MFP2 increased the growth rate.

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24

Butte, Manish, and Tim Thauland. "The actin capping protein alpha-adducin is required for CD28 costimulation (IRM12P.658)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 133.17. http://dx.doi.org/10.4049/jimmunol.194.supp.133.17.

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Abstract Alpha-adducin (Add1) is a critical component of the actin-spectrin network, acting to cap the barbed ends of actin filaments, and recruiting spectrin to these junctions. Add1 is expressed at high levels in naïve T cells and is down-modulated upon TCR stimulation, but the role that Add1 plays in the cytoskeletal rearrangements that occur in motile T cells and during immunological synapse formation have not been investigated. Using CD4 T cells from knockout mice, we show that Add1 is necessary for complete activation of T cells in response to low levels of antigen, as measured by proliferation and cytokine production. Interestingly, the defective proliferation we observed in Add1-/- T cells was due to an inability to respond to respond to CD28 costimulatory signals. Additionally, we demonstrate that naïve and recently activated T cells lacking Add1 have a defect in motility. Using CD4 T cells transduced with GFP-tagged Add1, we found that Add1 is located cortically in non-motile cells, but rapidly moves to the nascent uropod in T cells initiating a crawling phenotype. While the bulk of GFP-Add1 is located in the uropod of crawling cells, brief accumulations are seen at the leading edge. Real-time imaging of interactions between transduced T cells and peptide-loaded antigen presenting cells revealed that Add1 becomes concentrated at the distal pole complex. Together, these results demonstrate that Add1 plays an unexpected and central role in T cell activation and migration.

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25

Alama-Bermejo, Gema, Astrid S. Holzer, and Jerri L. Bartholomew. "Myxozoan Adhesion and Virulence: Ceratonova shasta on the Move." Microorganisms 7, no. 10 (September 26, 2019): 397. http://dx.doi.org/10.3390/microorganisms7100397.

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Motility factors are fundamental for parasite invasion, migration, proliferation and immune evasion and thus can influence parasitic disease pathogenesis and virulence. Salmonid enteronecrosis is caused by a myxozoan (Phylum Cnidarian) parasite, Ceratonova shasta. Three parasite genotypes (0, I, II) occur, with varying degrees of virulence in its host, making it a good model for examining the role of motility in virulence. We compare C. shasta cell motility between genotypes and describe how the cellular protrusions interact with the host. We support these observations with motility gene expression analyses. C. shasta stages can move by single or combined used of filopodia, lamellipodia and blebs, with different behaviors such as static adhesion, crawling or blebbing, some previously unobserved in myxozoans. C. shasta stages showed high flexibility of switching between different morphotypes, suggesting a high capacity to adapt to their microenvironment. Exposure to fibronectin showed that C. shasta stages have extraordinary adhesive affinities to glycoprotein components of the extracellular matrix (ECM). When comparing C. shasta genotypes 0 (low virulence, no mortality) and IIR (high virulence, high mortality) infections in rainbow trout, major differences were observed with regard to their migration to the target organ, gene expression patterns and proliferation rate in the host. IIR is characterized by rapid multiplication and fast amoeboid bleb-based migration to the gut, where adhesion (mediated by integrin-β and talin), ECM disruption and virulent systemic dispersion of the parasite causes massive pathology. Genotype 0 is characterized by low proliferation rates, slow directional and early adhesive migration and localized, non-destructive development in the gut. We conclude that parasite adhesion drives virulence in C. shasta and that effectors, such as integrins, reveal themselves as attractive therapeutic targets in a group of parasites for which no effective treatments are known.

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Waite, Janelle, Ingrid Leiner, Peter Lauer, Huan Zheng, Chris Rae, Daniel Portnoy, Eric Pamer, and Michael Dustin. "Intravital imaging of lymphocyte dynamics and signaling during immune Response to Listeria infection in the spleen (37.31)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 37.31. http://dx.doi.org/10.4049/jimmunol.184.supp.37.31.

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Abstract T cells play a major role in the adaptive immune response. T cells are primed by professional antigen presenting cells (APC), frequently dendritic cells (DC). T-DC interactions occur in lymphoid tissue where T cells are highly motile. Activation of the T cell receptor by cognate antigen triggers arrest in motility to allow stable and specialized contact with APC, termed the immunological synapse. Signaling that initiates and maintains stable T-DC contact has yet to be fully characterized. We employed intravital microscopy to image lymphocyte dynamics in the spleen, a major secondary lymphoid organ important for clearance of blood borne pathogens. We directly image a DC network in the subcapsular red pulp (scDC) where effector T cells migrate and arrest acutely in response to antigen. scDC internalized intravascular Listeria. Myelomonocytic cells were recruited and interdigitated with non-motile infected scDC as dynamic swarms and tight foci to contain Lm. Effector CD8+ T cells displayed a two-tiered reduction in motility with antigen independent and dependent components, including stable interactions with scDC. In addition, we monitored antigen induced intracellular calcium ([Ca2+]i) elevation in vivo. While [Ca2+]i elevation is sufficient to arrest crawling T cells, blocking [Ca2+]i elevation did not inhibit arrest. These data suggest there is an alternative antigen induced stopping pathway that allows stable T-APC contacts in the absence of [Ca2+]i elevation.

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Tal, Orna, Hwee Ying Lim, Irina Gurevich, Idan Milo, Zohar Shipony, Lai Guan Ng, Veronique Angeli, and Guy Shakhar. "DC mobilization from the skin requires docking to immobilized CCL21 on lymphatic endothelium and intralymphatic crawling." Journal of Experimental Medicine 208, no. 10 (September 19, 2011): 2141–53. http://dx.doi.org/10.1084/jem.20102392.

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Dendritic cells (DCs) must travel through lymphatics to carry skin antigens into lymph nodes. The processes controlling their mobilization and migration have not been completely delineated. We studied how DCs in live mice respond to skin inflammation, transmigrate through lymphatic endothelium, and propagate in initial lymphatics. At steady state, dermal DCs remain sessile along blood vessels. Inflammation mobilizes them, accelerating their interstitial motility 2.5-fold. CCR7-deficient BMDCs crawl as fast as wild-type DCs but less persistently. We observed discrete depositions of CCL21 complexed with collagen-IV on the basement membrane of initial lymphatics. Activated DCs move directionally toward lymphatics, contact CCL21 puncta, and migrate through portals into the lumen. CCR7-deficient DCs arrive at lymphatics through random migration but fail to dock and transmigrate. Once inside vessels, wild-type DCs use lamellipodia to crawl along lymphatic endothelium and, sensing lymph flow, proceed downstream. DCs start drifting freely only in collecting lymphatics. These results demonstrate in vivo that the CCL21–CCR7 axis plays a dual role in DC mobilization: promoting both chemotaxis and arrest of DCs on lymphatic endothelium. Intralymphatic crawling, in which DCs combine active adhesion-based migration and directional cues from lymph flow, represents a new step in DC mobilization which may be amenable to regulation.

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Stramer, Brian, Will Wood, Michael J. Galko, Michael J. Redd, Antonio Jacinto, Susan M. Parkhurst, and Paul Martin. "Live imaging of wound inflammation in Drosophila embryos reveals key roles for small GTPases during in vivo cell migration." Journal of Cell Biology 168, no. 4 (February 7, 2005): 567–73. http://dx.doi.org/10.1083/jcb.200405120.

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Aa robust inflammatory response to tissue damage and infection is conserved across almost all animal phyla. Neutrophils and macrophages, or their equivalents, are drawn to the wound site where they engulf cell and matrix debris and release signals that direct components of the repair process. This orchestrated cell migration is clinically important, and yet, to date, leukocyte chemotaxis has largely been studied in vitro. Here, we describe a genetically tractable in vivo wound model of inflammation in the Drosophila melanogaster embryo that is amenable to cinemicroscopy. For the first time, we are able to examine the roles of Rho-family small GTPases during inflammation in vivo and show that Rac-mediated lamellae are essential for hemocyte motility and Rho signaling is necessary for cells to retract from sites of matrix– and cell–cell contacts. Cdc42 is necessary for maintaining cellular polarity and yet, despite in vitro evidence, is dispensable for sensing and crawling toward wound cues.

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29

Adachi, Taiji, Kennedy O. Okeyo, Yoshimichi Shitagawa, and Masaki Hojo. "2P254 Strain Field Measurement of Cytoskeletal Actin Network in Lamellipodia of Crawling Fish Keratocytes(39. Cell motility,Poster Session,Abstract,Meeting Program of EABS & BSJ 2006)." Seibutsu Butsuri 46, supplement2 (2006): S359. http://dx.doi.org/10.2142/biophys.46.s359_2.

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30

Tarr, D. E. K., and Alan L. Scott. "MSP domain protein-1 from Ascaris suum and its possible role in the regulation of major sperm protein-based crawling motility." Molecular and Biochemical Parasitology 143, no. 2 (October 2005): 165–72. http://dx.doi.org/10.1016/j.molbiopara.2005.05.013.

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31

BIGNOLD, L. "Crawling-like movements of polymorphonuclear leukocytes in plasma are not a good index of their motility in microporous cellulose acetate membrane." Cell Biology International Reports 10, no. 7 (July 1986): 535–43. http://dx.doi.org/10.1016/0309-1651(86)90028-7.

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32

Verkhovsky, Alexander B., Oleg Y. Chaga, Sébastien Schaub, Tatyana M. Svitkina, Jean-Jacques Meister, and Gary G. Borisy. "Orientational Order of the Lamellipodial Actin Network as Demonstrated in Living Motile Cells." Molecular Biology of the Cell 14, no. 11 (November 2003): 4667–75. http://dx.doi.org/10.1091/mbc.e02-10-0630.

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Lamellipodia of crawling cells represent both the motor for cell advance and the primary building site for the actin cytoskeleton. The organization of actin in the lamellipodium reflects actin dynamics and is of critical importance for the mechanism of cell motility. In previous structural studies, the lamellipodial actin network was analyzed primarily by electron microscopy (EM). An understanding of lamellipodial organization would benefit significantly if the EM data were complemented and put into a kinetic context by establishing correspondence with structural features observable at the light microscopic level in living cells. Here, we use an enhanced phase contrast microscopy technique to visualize an apparent long-range diagonal actin meshwork in the advancing lamellipodia of living cells. Visualization of this meshwork permitted a correlative light and electron microscopic approach that validated the underlying organization of lamellipodia. The linear features in the light microscopic meshwork corresponded to regions of greater actin filament density. Orientation of features was analyzed quantitatively and compared with the orientation of actin filaments at the EM level. We infer that the light microscopic meshwork reflects the orientational order of actin filaments which, in turn, is related to their branching angle.

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33

Soll, David R., Deborah Wessels, Paul J. Heid, and Edward Voss. "Computer-Assisted Reconstruction and Motion Analysis of the Three-Dimensional Cell." Scientific World JOURNAL 3 (2003): 827–41. http://dx.doi.org/10.1100/tsw.2003.70.

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Even though several microscopic techniques provide three-dimensional (3D) information on fixed and living cells, the perception persists that cells are two-dimensional (2D). Cells are, in fact, 3D and their behavior, including the extension of pseudopods, includes an important 3D component. Although treating the cell as a 2D entity has proven effective in understanding how cells locomote, and in identifying defects in a variety of mutant and abnormal cells, there are cases in which 3D reconstruction and analysis are essential. Here, we describe advanced computer-assisted 3D reconstruction and motion analysis programs for both individual live, crawling cells and developing embryos. These systems (3D-DIAS, 3D-DIASemb) can be used to reconstruct and motion analyze at short time intervals the nucleus and pseudopodia as well as the entire surface of a single migrating cell, or every cell and nucleus in a developing embryo. Because all images are converted to mathematical representations, a variety of motility and dynamic morphology parameters can be computed that have proven quite valuable in the identification of mutant behaviors. We also describe examples of mutant behaviors in Dictyostelium that were revealed through 3D analysis.

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Wessels, D., J. Reynolds, O. Johnson, E. Voss, R. Burns, K. Daniels, E. Garrard, T. J. O'Halloran, and D. R. Soll. "Clathrin plays a novel role in the regulation of cell polarity, pseudopod formation, uropod stability and motility in Dictyostelium." Journal of Cell Science 113, no. 1 (January 1, 2000): 21–36. http://dx.doi.org/10.1242/jcs.113.1.21.

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Although the traditional role of clathrin has been in vesicle trafficking and the internalization of receptors, a novel role in cytokinesis was recently revealed in an analysis of a clathrin-minus Dictyostelium mutant (chc(-)). chc(-) cells grown in suspension were demonstrated to be defective in assembling myosin II into a normal contractile ring. To test whether this defect reflected a more general one of cytoskeletal dysfunction, chc(-) cells were analyzed for cell polarity, pseudopod formation, uropod stability, cell locomotion, chemotaxis, cytoskeletal organization and vesicle movement. chc(-) cells crawled, chemotaxed, localized F-actin in pseudopods, organized their microtubule cytoskeleton in a relatively normal fashion and exhibited normal vesicle dynamics. Although chc(-) cells extended pseudopods from the anterior half of the cell with the same frequency as normal chc(+) cells, they extended pseudopods at twice the normal frequency from the posterior half of the cell. The uropods of chc(-) cells also exhibited spatial instability. These defects resulted in an increase in roundness, a reduction in polarity, a reduction in velocity, a dramatic increase in turning, a high frequency of 180 degrees direction reversals and a decrease in the efficiency of chemotaxis. All defects were reversed in a rescued strain. These results are the first to suggest a novel role for clathrin in cell polarity, pseudopod formation, uropod stability and locomotion. It is hypothesized that clathrin functions to suppress pseudopod formation and to stabilize the uropod in the posterior half of a crawling cell, two behavioral characteristics that are essential for the maintenance of cellular polarity, efficient locomotion and efficient chemotaxis.

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35

Yi, Kexi, Shawnna M. Buttery, Murray Stewart, and Thomas M. Roberts. "A Ser/Thr Kinase Required for Membrane-associated Assembly of the Major Sperm Protein Motility Apparatus in the Amoeboid Sperm of Ascaris." Molecular Biology of the Cell 18, no. 5 (May 2007): 1816–25. http://dx.doi.org/10.1091/mbc.e06-08-0741.

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Leading edge protrusion in the amoeboid sperm of Ascaris suum is driven by the localized assembly of the major sperm protein (MSP) cytoskeleton in the same way that actin assembly powers protrusion in other types of crawling cell. Reconstitution of this process in vitro led to the identification of two accessory proteins required for MSP polymerization: an integral membrane phosphoprotein, MSP polymerization–organizing protein (MPOP), and a cytosolic component, MSP fiber protein 2 (MFP2). Here, we identify and characterize a 34-kDa cytosolic protein, MSP polymerization–activating kinase (MPAK) that links the activities of MPOP and MFP2. Depletion/add-back assays of sperm extracts showed that MPAK, which is a member of the casein kinase 1 family of Ser/Thr protein kinases, is required for motility. MPOP and MPAK comigrated by native gel electrophoresis, coimmunoprecipitated, and colocalized by immunofluorescence, indicating that MPOP binds to and recruits MPAK to the membrane surface. MPAK, in turn, phosphorylated MFP2 on threonine residues, resulting in incorporation of MFP2 into the cytoskeleton. Beads coated with MPAK assembled a surrounding cloud of MSP filaments when incubated in MPAK-depleted sperm extract, but only when supplemented with detergent-solubilized MPOP. Our results suggest that interactions involving MPOP, MPAK, and MFP2 focus MSP polymerization to the plasma membrane at the leading edge of the cell thereby generating protrusion and minimizing nonproductive filament formation elsewhere.

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Biesieda, Volodymyr. "Peculiarities of the mental and motility state of the children suffering from mental retardation and postural disorders." Scientific bulletin of South Ukrainian National Pedagogical University named after K. D. Ushynsky 2020, no. 4 (133) (December 24, 2020): 56–63. http://dx.doi.org/10.24195/2617-6688-2020-4-7.

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Nowadays, there are numerous scientific reviews and studies devoted to the problem of psychomotor retardation of children of different ages. Though, a comprehensive solution of how to identify psychophysical characteristics demonstrated by this category of small children suffering from postural disorders has not made yet. The goal of our research was to identify features of the mental and motility state of small children suffering from psychomotor retardation and postural disorders. Summarising the research performed, these conclusions have been made: The children demonstrating psychomotor retardation have different types of mental and somatic dysontogenesis, which negatively affects their academic performance and social adaptation; in the process of pedagogical observations, the small children suffering from psychomotor retardation and postural disorders demonstrate certain mental features in comparison with their healthy as follows: reduced motor-game activity, reduced participation as a leader in collective active games; lack of speech communication with peers, emotional instability, the children constituting this category fail to respond to changes in plot collisions of a game in time, in contradistinction to their healthy peers; their responses happen to be inadequate; they do not understand the rules of a game, or details of the game plot; do not always respond correctly to the results of the game commented by their teacher in each particular case; this category of children demonstrates specific peculiarities of their motor development: a reduced total volume of their daily locomotion compared to their healthy peers; these children prefer horizontal basic motor modes (lying, crawling, sitting), avoiding vertical gravitational starting positions; in case these children take vertical positions, they reflexively try to find additional support for the upper extremities or corpora; a reduced amount of purposeful motor-game actions with increased spontaneous motor activities; the movements of the children suffering from psychomotor retardation and postural disorders are often insufficiently coordinated by them; the problems causing fusion of movements should also be noted; insufficient rationality of motor actions performed by these children according to all the parameters (space-, time- and energy-related) is revealed. The prospects of further research in this area are seen in the study of physical, psycho-somatic and mental relationships alongside their impact on the overall development of small children suffering from mental retardation and postural disorders.

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Estin, Miriam L., Scott B. Thompson, Brianna Traxinger, Marlie H. Fisher, Rachel S. Friedman, and Jordan Jacobelli. "Ena/VASP proteins regulate activated T-cell trafficking by promoting diapedesis during transendothelial migration." Proceedings of the National Academy of Sciences 114, no. 14 (March 20, 2017): E2901—E2910. http://dx.doi.org/10.1073/pnas.1701886114.

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Vasodilator-stimulated phosphoprotein (VASP) and Ena-VASP–like (EVL) are cytoskeletal effector proteins implicated in regulating cell morphology, adhesion, and migration in various cell types. However, the role of these proteins in T-cell motility, adhesion, and in vivo trafficking remains poorly understood. This study identifies a specific role for EVL and VASP in T-cell diapedesis and trafficking. We demonstrate that EVL and VASP are selectively required for activated T-cell trafficking but are not required for normal T-cell development or for naïve T-cell trafficking to lymph nodes and spleen. Using a model of multiple sclerosis, we show an impairment in trafficking of EVL/VASP-deficient activated T cells to the inflamed central nervous system of mice with experimental autoimmune encephalomyelitis. Additionally, we found a defect in trafficking of EVL/VASP double-knockout (dKO) T cells to the inflamed skin and secondary lymphoid organs. Deletion of EVL and VASP resulted in the impairment in α4 integrin (CD49d) expression and function. Unexpectedly, EVL/VASP dKO T cells did not exhibit alterations in shear-resistant adhesion to, or in crawling on, primary endothelial cells under physiologic shear forces. Instead, deletion of EVL and VASP impaired T-cell diapedesis. Furthermore, T-cell diapedesis became equivalent between control and EVL/VASP dKO T cells upon α4 integrin blockade. Overall, EVL and VASP selectively mediate activated T-cell trafficking by promoting the diapedesis step of transendothelial migration in a α4 integrin-dependent manner.

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Varkey, J. P., P. L. Jansma, A. N. Minniti, and S. Ward. "The Caenorhabditis elegans spe-6 gene is required for major sperm protein assembly and shows second site non-complementation with an unlinked deficiency." Genetics 133, no. 1 (January 1, 1993): 79–86. http://dx.doi.org/10.1093/genetics/133.1.79.

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Abstract Caenorhabditis elegans spermatozoa move by crawling. Their motility requires thin cytoskeletal filaments assembled from a unique cytoskeletal protein, the major sperm protein (MSP). During normal sperm development the MSP is segregated to developing sperm by assembly into filaments that form a paracrystalline array in a transient organelle, the fibrous body-membranous organelle. Mutations in the spe-6 gene cause sterility because they lead to defective primary spermatocytes that do not form spermatids. In these mutant spermatocytes the MSP fails to assemble into fibrous body filaments. Instead, the unassembled MSP distributes throughout the cytoplasm and nucleus. Thus, the spe-6 gene product is necessary for normal MSP localization and assembly during sperm development. In addition to their MSP assembly defect, spe-6 mutant spermatocytes arrest meiosis at diakinesis although their spindle pole bodies still replicate and separate. This results in spermatocytes with four half-spindles surrounding condensed, but unsegregated, chromosomes. All four spe-6 alleles, as well as a chromosome III deficiency that deletes the spe-6 gene, fail to complement two small overlapping chromosome IV deficiencies, eDf18 and eDf19. This non-allele-specific second site non-complementation suggests a concentration-dependent interaction between the spe-6 gene product and products of the gene(s) under eDf18 and eDf19, which include a cluster of sperm-specific genes. Since MSP filament assembly is highly concentration-dependent in vitro, the non-complementation might be expected if the sperm-specific gene products under eDf18 and eDf19 were needed together with the spe-6 gene product to promote MSP assembly.

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Magdalena, Juana, Thomas H. Millard, Sandrine Etienne-Manneville, Sophie Launay, Helen K. Warwick, and Laura M. Machesky. "Involvement of the Arp2/3 Complex and Scar2 in Golgi Polarity in Scratch Wound Models." Molecular Biology of the Cell 14, no. 2 (February 2003): 670–84. http://dx.doi.org/10.1091/mbc.e02-06-0345.

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Cell motility and cell polarity are essential for morphogenesis, immune system function, and tissue repair. Many animal cells move by crawling, and one main driving force for movement is derived from the coordinated assembly and disassembly of actin filaments. As tissue culture cells migrate to close a scratch wound, this directional extension is accompanied by Golgi apparatus reorientation, to face the leading wound edge, giving the motile cell inherent polarity aligned relative to the wound edge and to the direction of cell migration. Cellular proteins essential for actin polymerization downstream of Rho family GTPases include the Arp2/3 complex as an actin nucleator and members of the Wiskott–Aldrich Syndrome protein (WASP) family as activators of the Arp2/3 complex. We therefore analyzed the involvement of the Arp2/3 complex and WASP-family proteins in in vitro wound healing assays using NIH 3T3 fibroblasts and astrocytes. In NIH 3T3 cells, we found that actin and Arp2/3 complex contributed to cell polarity establishment. Moreover, overexpression of N-terminal fragments of Scar2 (but not N-WASP or Scar1 or Scar3) interfere with NIH 3T3 Golgi polarization but not with cell migration. In contrast, actin, Arp2/3, and WASP-family proteins did not appear to be involved in Golgi polarization in astrocytes. Our results thus indicate that the requirement for Golgi polarity establishment is cell-type specific. Furthermore, in NIH 3T3 cells, Scar2 and the Arp2/3 complex appear to be involved in the establishment and maintenance of Golgi polarity during directed migration.

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BORODAI, E. "MILITARYAPPLIED SPORTS AS EFFECTIVE MEANS OF DEVELOPMENT OF MOTILITY OF MOVEMENTS AND FORMATION OF APPLIED SKILLS OF HIGH SCHOOL STUDENT IN THE PROCESS OF PRECONSCRIPTION TRAINING." Pedagogical Sciences, no. 75-76 (December 12, 2020): 44–49. http://dx.doi.org/10.33989/2524-2474.2020.75-76.226366.

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The theoretical bases of application of military-applied sports as effective means of development of physical skills of senior pupils in the course of pre-conscription preparation are considered in the article. It was found that the correct influence on physiological development forms the general moral and psychological readiness of the soldier. The most effective means of physical training of high school students during pre-service training is the introduction of military-applied sports in the educational process, among which the leading place is occupied by military sports, which have a complex impact on the development of high school students. military applied skills and abilities. Modern scientists have found that modern methods and systems of all-around competitions are best adapted to the real conditions of battle, so not only increase the level of physical fitness of future recruits, but also improve their moral and psychological condition on the battlefield. The article also identifies a set of exercises that have a direct impact on the formation of volitional and emotional stability of the serviceman. In particular, the educationof courage and determination is carried out during the performance of tasks that are new to perform, in particular walking on logs, stumps; overcoming high-altitude obstacles; jumping over trenches, fences; climbing high obstacles; jumping into the water, overcoming water obstacles. The development of initiative, ingenuity and ingenuity occurs in the process of solving problems that require independent decision-making: overcoming areas of confined space; diving to length in uniform; dogfight. Exercises that involve significant and prolonged physical exertion and psychological stress, such as march-throw, which is combined with overcoming obstacles, transporting the wounded, carrying boxes, dragging bags; crawling like a platoon in difficult weather conditions, cultivate perseverance and perseverance in the military. Performing exercises that require precision of movement, despite physical exertion and mental stress, and occur in the rapid dynamics of change (swimming in equipment and with weapons; practice in the water while overcoming water obstacles; delayed breathing under water; staying in the cold for a long time water, overcoming the elements of the psychological barrier) contribute to the development of endurance and self-control.

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Sakai, Tatsuya, Hiroaki Takagi, Yasushi Muraki, and Mineki Saito. "Unique Directional Motility of Influenza C Virus Controlled by Its Filamentous Morphology and Short-Range Motions." Journal of Virology 92, no. 2 (November 8, 2017). http://dx.doi.org/10.1128/jvi.01522-17.

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ABSTRACT Influenza virus motility is based on cooperation between two viral spike proteins, hemagglutinin (HA) and neuraminidase (NA), and is a major determinant of virus infectivity. To translocate a virus particle on the cell surface, HA molecules exchange viral receptors and NA molecules accelerate the receptor exchange of HA. This type of virus motility was recently identified in influenza A virus (IAV). To determine if other influenza virus types have a similar receptor exchange mechanism-driven motility, we investigated influenza C virus (ICV) motility on a receptor-fixed glass surface. This system excludes receptor mobility, which makes it more desirable than a cell surface for demonstrating virus motility by receptor exchange. Like IAV, ICV was observed to move across the receptor-fixed surface. However, in contrast to the random movement of IAV, a filamentous ICV strain, Ann Arbor/1/50 (AA), moved in a straight line, in a directed manner, and at a constant rate, whereas a spherical ICV strain, Taylor/1233/47 (Taylor), moved randomly, similar to IAV. The AA and Taylor viruses each moved with a combination of gradual (crawling) and rapid (gliding) motions, but the distances of crawling and gliding for the AA virus were shorter than those of the Taylor virus. Our findings indicate that like IAV, ICV also has a motility that is driven by the receptor exchange mechanism. However, compared with IAV movement, filamentous ICV movement is highly regulated in both direction and speed. Control of ICV movement is based on its specific motility employing short crawling and gliding motions as well as its own filamentous morphology. IMPORTANCE Influenza virus enters into a host cell for infection via cellular endocytosis. Human influenza virus infects epithelial cells of the respiratory tract, the surfaces of which are hidden by abundant cilia that are inactive in endocytosis. An open question is the manner by which the virus migrates to endocytosis-active domains. In analyzing individual virus behaviors through single-virus tracking, we identified a novel function of the hemagglutinin and esterase of influenza C virus (ICV) as the motility machinery. Hemagglutinin iteratively exchanges a viral receptor, causing virus movement. Esterase degrades the receptors along the trajectory traveled by the virus and prevents the virus from moving backward, causing directional movement. We propose that ICV has a unique motile machinery directionally controlled via hemagglutinin sensing the receptor density manipulated by esterase.

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Kokubu, Eitoyo, Yuichiro Kikuchi, Kazuko Okamoto‐Shibayama, Shuichi Nakamura, and Kazuyuki Ishihara. "Crawling motility of Treponema denticola modulated by outer sheath protein." Microbiology and Immunology, September 9, 2021. http://dx.doi.org/10.1111/1348-0421.12940.

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43

DeSimone, A., and A. Tatone. "Crawling motility through the analysis of model locomotors: Two case studies." European Physical Journal E 35, no. 9 (September 2012). http://dx.doi.org/10.1140/epje/i2012-12085-x.

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44

Moreno-Cañadas, Rocío, Laura Luque-Martín, and Alicia G. Arroyo. "Intravascular Crawling of Patrolling Monocytes: A Lèvy-Like Motility for Unique Search Functions?" Frontiers in Immunology 12 (September 17, 2021). http://dx.doi.org/10.3389/fimmu.2021.730835.

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Patrolling monocytes (PMo) are the organism’s preeminent intravascular guardians by their continuous search of damaged endothelial cells and harmful microparticles for their removal and to restore homeostasis. This surveillance is accomplished by PMo crawling on the apical side of the endothelium through regulated interactions of integrins and chemokine receptors with their endothelial ligands. We propose that the search mode governs the intravascular motility of PMo in vivo in a similar way to T cells looking for antigen in tissues. Signs of damage to the luminal side of the endothelium (local death, oxidized LDL, amyloid deposits, tumor cells, pathogens, abnormal red cells, etc.) will change the diffusive random towards a Lèvy-like crawling enhancing their recognition and clearance by PMo damage receptors as the integrin αMβ2 and CD36. This new perspective can help identify new actors to promote unique PMo intravascular actions aimed at maintaining endothelial fitness and combating harmful microparticles involved in diseases as lung metastasis, Alzheimer’s angiopathy, vaso-occlusive disorders, and sepsis.

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45

Baum, Buzz, and Gautam Dey. "Moving simply: Naegleria crawls and feeds using an ancient Arp2/3-dependent mechanism." Journal of Cell Biology 219, no. 11 (October 16, 2020). http://dx.doi.org/10.1083/jcb.202009031.

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Arp2/3-nucleated actin filaments drive crawling motility and phagocytosis in animal cells and slime molds. In this issue, Velle and Fritz-Laylin (2020. J. Cell Biol.https://doi.org/10.1083/jcb.202007158) now show that Naegleria gruberi, belonging to a lineage that diverged from opisthokonts around a billion years ago, uses similar mechanisms to crawl and phagocytose bacteria.

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46

Brunet, Thibaut, Marvin Albert, William Roman, Maxwell C. Coyle, Danielle C. Spitzer, and Nicole King. "A flagellate-to-amoeboid switch in the closest living relatives of animals." eLife 10 (January 15, 2021). http://dx.doi.org/10.7554/elife.61037.

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Amoeboid cell types are fundamental to animal biology and broadly distributed across animal diversity, but their evolutionary origin is unclear. The closest living relatives of animals, the choanoflagellates, display a polarized cell architecture (with an apical flagellum encircled by microvilli) that resembles that of epithelial cells and suggests homology, but this architecture differs strikingly from the deformable phenotype of animal amoeboid cells, which instead evoke more distantly related eukaryotes, such as diverse amoebae. Here, we show that choanoflagellates subjected to confinement become amoeboid by retracting their flagella and activating myosin-based motility. This switch allows escape from confinement and is conserved across choanoflagellate diversity. The conservation of the amoeboid cell phenotype across animals and choanoflagellates, together with the conserved role of myosin, is consistent with homology of amoeboid motility in both lineages. We hypothesize that the differentiation between animal epithelial and crawling cells might have evolved from a stress-induced switch between flagellate and amoeboid forms in their single-celled ancestors.

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47

Velle, Katrina B., and Lillian K. Fritz-Laylin. "Conserved actin machinery drives microtubule-independent motility and phagocytosis in Naegleria." Journal of Cell Biology 219, no. 11 (September 22, 2020). http://dx.doi.org/10.1083/jcb.202007158.

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Much of our understanding of actin-driven phenotypes in eukaryotes has come from the “yeast-to-human” opisthokont lineage and the related amoebozoa. Outside of these groups lies the genus Naegleria, which shared a common ancestor with humans >1 billion years ago and includes the “brain-eating amoeba.” Unlike nearly all other known eukaryotic cells, Naegleria amoebae lack interphase microtubules; this suggests that actin alone drives phenotypes like cell crawling and phagocytosis. Naegleria therefore represents a powerful system to probe actin-driven functions in the absence of microtubules, yet surprisingly little is known about its actin cytoskeleton. Using genomic analysis, microscopy, and molecular perturbations, we show that Naegleria encodes conserved actin nucleators and builds Arp2/3–dependent lamellar protrusions. These protrusions correlate with the capacity to migrate and eat bacteria. Because human cells also use Arp2/3–dependent lamellar protrusions for motility and phagocytosis, this work supports an evolutionarily ancient origin for these processes and establishes Naegleria as a natural model system for studying microtubule-independent cytoskeletal phenotypes.

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48

Camley, Brian A., Yanxiang Zhao, Bo Li, Herbert Levine, and Wouter-Jan Rappel. "Crawling and turning in a minimal reaction-diffusion cell motility model: Coupling cell shape and biochemistry." Physical Review E 95, no. 1 (January 5, 2017). http://dx.doi.org/10.1103/physreve.95.012401.

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49

Kempers, Lanette, Evelien G. G. Sprenkeler, Abraham C. I. van Steen, Jaap D. van Buul, and Taco W. Kuijpers. "Defective Neutrophil Transendothelial Migration and Lateral Motility in ARPC1B Deficiency Under Flow Conditions." Frontiers in Immunology 12 (May 31, 2021). http://dx.doi.org/10.3389/fimmu.2021.678030.

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The actin-related protein (ARP) 2/3 complex, essential for organizing and nucleating branched actin filaments, is required for several cellular immune processes, including cell migration and granule exocytosis. Recently, genetic defects in ARPC1B, a subunit of this complex, were reported. Mutations in ARPC1B result in defective ARP2/3-dependent actin filament branching, leading to a combined immunodeficiency with severe inflammation. In vitro, neutrophils of these patients showed defects in actin polymerization and chemotaxis, whereas adhesion was not altered under static conditions. Here we show that under physiological flow conditions human ARPC1B-deficient neutrophils were able to transmigrate through TNF-α-pre-activated endothelial cells with a decreased efficiency and, once transmigrated, showed definite impairment in subendothelial crawling. Furthermore, severe locomotion and migration defects were observed in a 3D collagen matrix and a perfusable vessel-on-a-chip model. These data illustrate that neutrophils employ ARP2/3-independent steps of adhesion strengthening for transmigration but rely on ARP2/3-dependent modes of migration in a more complex multidimensional environment.

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50

Xu, Jun, Nobuo Koizumi, and Shuichi Nakamura. "Crawling Motility on the Host Tissue Surfaces Is Associated With the Pathogenicity of the Zoonotic Spirochete Leptospira." Frontiers in Microbiology 11 (August 5, 2020). http://dx.doi.org/10.3389/fmicb.2020.01886.

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