The making of filopodia

Faix, Jan; Rottner, Klemens

doi:10.1016/j.ceb.2005.11.002

Cited by 301 publications

(296 citation statements)

References 62 publications

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“…In a polarized migrating cell, lamellipodia is highly active in defining the direction of the cell movement. Another type of leading edge structures, thin finger-like protrusions called filopodia, are believed to be responsible for exploring the environment during motility (Faix and Rottner, 2006;Gupton and Gertler, 2007). While it has been suggested that inhibition of lamellipodia (Gupton et al, 2005;Yang et al, 2007) or filopodia does not inhibit cell motility, it results in defects in cell migration speed and directionality.…”

Section: Basic Principles Of Cell Migration Overall Structure Of the mentioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

117

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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Section: Basic Principles Of Cell Migration Overall Structure Of the mentioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

117

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“…45 For example, RhoA is required for mDIA1-induced filopodia at the front of N-WASP/WAVEdepleted carcinoma cells. 37 Whilst it is not possible to look at the formation of filopodia during TEM in RhoA-depleted T cells as these cells do not initiate TEM, it would be interesting to examine whether proteins involved in filopodium formation in other cell types, such as vasodilator-stimulated phospho-protein (VASP), fascin, insulin receptor substrate p53 (IRSp53) and myosin X, 47 localize to the structures we observe in transmigrating T cells. The mDIA proteins are likely…”

Section: A Possible Role Of Rhoa In Filopodia During T Cell Temmentioning

confidence: 99%

Multiple roles for RhoA during T cell transendothelial migration

Heasman

Ridley

2010

Small GTPases

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t cells need to cross endothelial barriers during immune surveillance and inflammation. this involves t-cell adhesion to the endothelium followed by polarization and crawling with a lamellipodium at the front and contractile uropod at the back. t cells subsequently extend lamellipodia and filopodia under the endothelium in order to transmigrate. rho Gtpases play key roles in cell migration by regulating cytoskeletal dynamics and cell adhesion. we have found that the rho Gtpase rhoa is required for efficient t-cell polarization and migration on endothelial cells as well as transendothelial migration. rhoa-depleted cells lack both lamellipodia and uropods, and instead have narrow protrusions extending from a rounded cell body. using a rhoa activity biosensor, we have shown that rhoa is active at the leading edge in lamellipodia and filopodia of crawling and transmigrating t cells, as well as in the uropod. in lamellipodia, its activity correlates with both protrusion and retraction. we predict that rhoa signals via the formin mdia1 during lamellipodial protrusion whereas it induces lamellipodial retraction via the kinase rocK and actomyosin contractility. we propose that different guanine-nucleotide exchange factors (GEfs) are responsible for coordinating rhoa activation and signaling in different regions of transmigrating t cells. IntroductionDuring inflammation leukocytes are recruited from the vasculature into tissues using a specialized migratory pathway. Rho GTPase family proteins are key regulators of cytoskeletal dynamics and cell migration, 3 and thus would be expected to contribute to the process of TEM. Most Rho GTPases cycle between an inactive, GDP-bound form and an active, GTP-bound form, which interacts with and activates downstream targets. Rho GTPases are stimulated by guanine nucleotide exchange factors (GEFs), which stimulate exchange of GDP for GTP and inactivated by GTPaseactivating proteins (GAPs), which stimulate GTP hydrolysis.In our recent paper we used an RNAi screen to identify which Rho GTPases are important for T cell TEM. 4 We found that knockdown of RhoA induced the strongest inhibition of this process and so subsequently examined the role of RhoA in detail during both T cell crawling on EC and subsequent TEM. Significantly, active RhoA was observed at both the front and back of polarized T cells as they crawled on EC and transmigrated, as well as in dynamic puncta in the basal membrane and filopodia extending beneath the endothelium of transmigrating cells ( fig. 1). Here we discuss the implications of these findings in the context of current understanding of RhoA signaling and the potential function of these cellular processes in T-cell migration. Extra View to: Heasman SJ, Carlin LM, Cox S, Ng T, Ridley AJ. Coordinated RhoA signaling at the leading edge and uropod is required for T cell transendothelial migration.

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“…3C). 22 The platelet filopodia consist of actin filaments that are shorter than an entire filopod and are in parallel or oblique to the filopod's axis. Furthermore, a large number of densities are detected at the plasma membrane (Fig.…”

Section: Zooming Into Intact Platelets With Cryo-electron Tomographymentioning

confidence: 99%

Toward correlating structure and mechanics of platelets

Sorrentino

Studt

Horev

et al. 2016

Cell Adhesion & Migration

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The primary physiological function of blood platelets is to seal vascular lesions after injury and form hemostatic thrombi in order to prevent blood loss. This task relies on the formation of strong cellular-extracellular matrix interactions in the subendothelial lesions. The cytoskeleton of a platelet is key to all of its functions: its ability to spread, adhere and contract. Despite the medical significance of platelets, there is still no high-resolution structural information of their cytoskeleton. Here, we discuss and present 3-dimensional (3D) structural analysis of intact platelets by using cryoelectron tomography (cryo-ET) and atomic force microscopy (AFM). Cryo-ET provides in situ structural analysis and AFM gives stiffness maps of the platelets. In the future, combining highresolution structural and mechanical techniques will bring new understanding of how structural changes modulate platelet stiffness during activation and adhesion.

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The making of filopodia

Cited by 301 publications

References 62 publications

Cell biology of embryonic migration

Cell biology of embryonic migration

Multiple roles for RhoA during T cell transendothelial migration

Toward correlating structure and mechanics of platelets

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