Formins and VASPs may co-operate in the formation of filopodia

2005 ◽  
Vol 33 (6) ◽  
pp. 1256-1259 ◽  
Author(s):  
A. Schirenbeck ◽  
R. Arasada ◽  
T. Bretschneider ◽  
M. Schleicher ◽  
J. Faix
Keyword(s):  
Actin Filaments ◽  
Actin Polymerization ◽  
Cell Types ◽  
Binding Partner ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Dynamic Structures ◽  
Parallel Arrays ◽  
Cell Substrate Adhesion

Filopodia are finger-like cell protrusions composed of parallel arrays of actin filaments, which elongate through actin polymerization at their tips. These highly dynamic structures seem to be used by many cell types as sensing organs to explore environmental cues and have been implicated in cell motility as well as in cell–substrate adhesion. Formins are highly conserved multidomain proteins that play important roles in the nucleation of actin and the formation of linear actin filaments, yet their role in filopodia formation has remained poorly defined. The Dictyostelium diaphanous-related formin dDia2 is strongly enriched in filopodia tips. Genetic and biochemical analysis revealed that this protein is important for cell migration and cell adhesion, but most importantly for the formation of filopodia. Recently, we have identified the Dictyostelium VASP (vasodilator-stimulated phosphoprotein) orthologue as a binding partner of dDia2 and provide evidence for a co-operative role of both proteins in filopodia formation.

scholarly journals The crosstalk between microtubules, actin and membranes shapes cell division

Open Biology ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 190314 ◽  
Author(s):  
Francesca Rizzelli ◽  
Maria Grazia Malabarba ◽  
Sara Sigismund ◽  
Marina Mapelli
Keyword(s):  
Membrane Trafficking ◽  
Mitotic Progression ◽  
Isolated Cells ◽  
Spindle Positioning ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Epithelial Sheets ◽  
Cell Substrate Adhesion ◽  
Extracellular Signalling

Mitotic progression is orchestrated by morphological and mechanical changes promoted by the coordinated activities of the microtubule (MT) cytoskeleton, the actin cytoskeleton and the plasma membrane (PM). MTs assemble the mitotic spindle, which assists sister chromatid separation, and contact the rigid and tensile actomyosin cortex rounded-up underneath the PM. Here, we highlight the dynamic crosstalk between MTs, actin and cell membranes during mitosis, and discuss the molecular connections between them. We also summarize recent views on how MT traction forces, the actomyosin cortex and membrane trafficking contribute to spindle positioning in isolated cells in culture and in epithelial sheets. Finally, we describe the emerging role of membrane trafficking in synchronizing actomyosin tension and cell shape changes with cell–substrate adhesion, cell–cell contacts and extracellular signalling events regulating proliferation.

scholarly journals The interplay of cell–cell and cell–substrate adhesion in collective cell migration

2014 ◽  
Vol 11 (100) ◽  
pp. 20140684 ◽  
Author(s):  
Chenlu Wang ◽  
Sagar Chowdhury ◽  
Meghan Driscoll ◽  
Carole A. Parent ◽  
S. K. Gupta ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Actin Polymerization ◽  
Collective Cell Migration ◽  
Cell Contacts ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Shapes ◽  
Cell Substrate Adhesion ◽  
Cell Cell

Collective cell migration often involves notable cell–cell and cell–substrate adhesions and highly coordinated motion of touching cells. We focus on the interplay between cell–substrate adhesion and cell–cell adhesion. We show that the loss of cell-surface contact does not significantly alter the dynamic pattern of protrusions and retractions of fast migrating amoeboid cells ( Dictyostelium discoideum ), but significantly changes their ability to adhere to other cells. Analysis of the dynamics of cell shapes reveals that cells that are adherent to a surface may coordinate their motion with neighbouring cells through protrusion waves that travel across cell–cell contacts. However, while shape waves exist if cells are detached from surfaces, they do not couple cell to cell. In addition, our investigation of actin polymerization indicates that loss of cell-surface adhesion changes actin polymerization at cell–cell contacts. To further investigate cell–cell/cell–substrate interactions, we used optical micromanipulation to form cell–substrate contact at controlled locations. We find that both cell-shape dynamics and cytoskeletal activity respond rapidly to the formation of cell–substrate contact.

scholarly journals The Role of Mitotic Cell-Substrate Adhesion Re-modeling in Animal Cell Division

2018 ◽  
Vol 45 (1) ◽  
pp. 132-145.e3 ◽  
Author(s):  
Christina L. Dix ◽  
Helen K. Matthews ◽  
Marina Uroz ◽  
Susannah McLaren ◽  
Lucie Wolf ◽  
...  
Keyword(s):  
Cell Division ◽  
Animal Cell ◽  
Mitotic Cell ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Substrate Adhesion

scholarly journals Actin flow and talin dynamics govern rigidity sensing in actin–integrin linkage through talin extension

2014 ◽  
Vol 11 (99) ◽  
pp. 20140734 ◽  
Author(s):  
Hiroaki Hirata ◽  
Keng-Hwee Chiam ◽  
Chwee Teck Lim ◽  
Masahiro Sokabe
Keyword(s):  
Actin Filaments ◽  
Substrate Stiffness ◽  
Mechanical Stiffness ◽  
Adhesion Sites ◽  
Substrate Adhesion ◽  
Rigidity Sensing ◽  
Cell Substrate ◽  
Simple Physical Model ◽  
Biophysical Mechanism ◽  
Cell Substrate Adhesion

At cell–substrate adhesion sites, the linkage between actin filaments and integrin is regulated by mechanical stiffness of the substrate. Of potential molecular regulators, the linker proteins talin and vinculin are of particular interest because mechanical extension of talin induces vinculin binding with talin, which reinforces the actin–integrin linkage. For understanding the molecular and biophysical mechanism of rigidity sensing at cell–substrate adhesion sites, we constructed a simple physical model to examine a role of talin extension in the stiffness-dependent regulation of actin–integrin linkage. We show that talin molecules linking between retrograding actin filaments and substrate-bound integrin are extended in a manner dependent on substrate stiffness. The model predicts that, in adhesion complexes containing ≈30 talin links, talin is extended enough for vinculin binding when the substrate is stiffer than 1 kPa. The lifetime of talin links needs to be 2–5 s to achieve an appropriate response of talin extension against substrate stiffness. Furthermore, changes in actin velocity drastically shift the range of substrate stiffness that induces talin–vinculin binding. Our results suggest that talin extension is a key step in sensing and responding to substrate stiffness at cell adhesion sites.

scholarly journals Paxillin and Phospholipase D Interact To Regulate Actin-Based Processes in Dictyostelium discoideum

2011 ◽  
Vol 10 (7) ◽  
pp. 977-984 ◽  
Author(s):  
Jelena Pribic ◽  
Rebecca Garcia ◽  
May Kong ◽  
Derrick Brazill
Keyword(s):  
Dictyostelium Discoideum ◽  
Phospholipase D ◽  
Actin Polymerization ◽  
Genetic Interaction ◽  
Actin Reorganization ◽  
Content Type ◽  
Multicellular Development ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Substrate Adhesion

ABSTRACT The actin cytoskeleton forms a membrane-associated network whose proper regulation is essential for numerous processes, including cell differentiation, proliferation, adhesion, chemotaxis, endocytosis, exocytosis, and multicellular development. In this report, we show that in Dictyostelium discoideum , paxillin (PaxB) and phospholipase D (PldB) colocalize and coimmunoprecipitate, suggesting that they interact physically. Additionally, the phenotypes observed during development, cell sorting, and several actin-required processes, including cyclic AMP (cAMP) chemotaxis, cell-substrate adhesion, actin polymerization, phagocytosis, and exocytosis, reveal a genetic interaction between paxB and pldB , suggesting a functional interaction between their gene products. Taken together, our data point to PldB being a required binding partner of PaxB during processes involving actin reorganization.

scholarly journals Regulation of epithelial cell organization by tuning cell–substrate adhesion

2015 ◽  
Vol 7 (10) ◽  
pp. 1228-1241 ◽  
Author(s):  
Andrea Ravasio ◽  
Anh Phuong Le ◽  
Thuan Beng Saw ◽  
Victoria Tarle ◽  
Hui Ting Ong ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Particle Image ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Image Velocimetry ◽  
Cell Organization ◽  
Cell Substrate Adhesion

Combining live cell imaging, particle image velocimetry and numerical simulations, we show the role of extracellular matrix and intercellular adhesion on the expansion of epithelial cells.

scholarly journals The Janus Role of Adhesion in Chondrogenesis

2020 ◽  
Vol 21 (15) ◽  
pp. 5269 ◽  
Author(s):  
Ignasi Casanellas ◽  
Anna Lagunas ◽  
Yolanda Vida ◽  
Ezequiel Pérez-Inestrosa ◽  
José A. Andrades ◽  
...  
Keyword(s):  
Cell Tracking ◽  
Tissue Adhesive ◽  
Pcr Analysis ◽  
Condensation Process ◽  
Local Surface ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Substrate Adhesion ◽  
Fluorescence Live Cell Imaging

Tackling the first stages of the chondrogenic commitment is essential to drive chondrogenic differentiation to healthy hyaline cartilage and minimize hypertrophy. During chondrogenesis, the extracellular matrix continuously evolves, adapting to the tissue adhesive requirements at each stage. Here, we take advantage of previously developed nanopatterns, in which local surface adhesiveness can be precisely tuned, to investigate its effects on prechondrogenic condensation. Fluorescence live cell imaging, immunostaining, confocal microscopy and PCR analysis are used to follow the condensation process on the nanopatterns. Cell tracking parameters, condensate morphology, cell–cell interactions, mechanotransduction and chondrogenic commitment are evaluated in response to local surface adhesiveness. Results show that only condensates on the nanopatterns of high local surface adhesiveness are stable in culture and able to enter the chondrogenic pathway, thus highlighting the importance of controlling cell–substrate adhesion in the tissue engineering strategies for cartilage repair.

scholarly journals Modeling cell-substrate de-adhesion dynamics under fluid shear

2017 ◽  
Author(s):  
Renu Maan ◽  
Garima Rani ◽  
Gautam I. Menon ◽  
Pramod A. Pullarkat
Keyword(s):  
Shear Stress ◽  
Cell Adhesion ◽  
Cancer Metastasis ◽  
Cell Types ◽  
Model Systems ◽  
Cell Detachment ◽  
Fluid Shear ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Substrate Adhesion

AbstractChanges in cell-substrate adhesion are believed to signal the onset of cancer metastasis, but such changes must be quantified against background levels of intrinsic heterogeneity between cells. Variations in cell-substrate adhesion strengths can be probed through biophysical measurements of cell detachment from substrates upon the application of an external force. Here, we investigate, theoretically and experimentally, the detachment of cells adhered to substrates when these cells are subjected to fluid shear. We present a theoretical framework within which we calculate the fraction of detached cells as a function of shear stress for fast ramps as well as for the decay in the fraction of detached cells at fixed shear stress as a function of time. Using HEK and 3T3 fibroblast cells as experimental model systems, we extract characteristic force scales for cell adhesion as well as characteristic detachment times. We estimate force-scales of ~ 500 pN associated to a single focal contact, and characteristic time-scales of 190 ≤ τ ≤ 350s representing cell-spread-area dependent mean first passage times to the detached state at intermediate values of the shear stress. Variations in adhesion across cell types are especially prominent when cell detachment is probed by applying a time-varying shear stress. These methods can be applied to characterizing changes in cell adhesion in a variety of contexts, including metastasis.

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