Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes
Open accessAbstract
Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion.
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Defects in neutrophil, dendritic cell, and macrophage migration and phagocytosis impair innate immune defenses, predisposing HEM1-deficient patients to bacterial infections.
“Like mouse models of HEM1 deficiency, defects in neutrophil, dendritic cell, and macrophage migration and phagocytosis impair innate immune defenses, predisposing patients to bacterial infections [32–35].”
From HEM1 Actin Immunodysregulatory Disorder: Genotypes, Phenotypes, and Future Directions (2022) · cites this paper as [35]
The paper’s account of the Figure 2 experiments reports impaired migration and lymphatic-vessel entry by Hem1-deficient mouse dendritic cells. It does not establish neutrophil or macrophage migration defects, phagocytosis defects, or that these changes predispose patients to bacterial infections. (LLM, conf=0.87)
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Kunda, P., Craig, G., Dominguez, V., & Baum, B. (2003) · Current Biology · doi:10.1016/j.cub.2003.10.005 · Cited by 341 · see citing works
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- Rotty, J. D., Wu, C. & Bear, J. E. New insights into the regulation and cellular functions of the ARP2/3 complex. Nat Rev Mol Cell Biol (2012). doi:10.1038/nrm3492 · DOI
- Suraneni, P. et al. The Arp2/3 complex is required for lamellipodia extension and directional fibroblast cell migration. The Journal of Cell Biology 197, 239-251 (2012).
- Renkawitz, J. et al. Adaptive force transmission in amoeboid cell migration. Nature Publishing Group 1-19 (2009). doi:10.1038/ncb1992 · DOI
- Redecke, V. et al. hematopoietic progenitor cell lines with myeloid and lymphoid potential. Nature Methods 1-13 (2013). doi:10.1038/nmeth.2510 · DOI
- Weiner, O. D. et al. Hem-1 Complexes Are Essential for Rac Activation, Actin Polymerization, and Myosin Regulation during Neutrophil Chemotaxis. PLoS Biol 4, e38 (2006).
- Svitkina, T. M. & Borisy, G. G. Arp2/3 complex and actin depolymerizing factor/cofilin in dendritic organization and treadmilling of actin filament array in lamellipodia. The Journal of Cell Biology 145, 1009-1026 (1999).
- Vinzenz, M. et al. Actin branching in the initiation and maintenance of lamellipodia. Journal of Cell Science 125, 2775-2785 (2012).
- Narita, A. et al. Direct Determination of Actin Polarity in the Cell. Journal of Molecular Biology 419, 359-368 (2012).
- Pflicke, H. & Sixt, M. Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels. Journal of Experimental Medicine 206, 2925-2935 (2009).
- Wolf, K. et al. Physical limits of cell migration: control by ECM space and nuclear deformation and tuning by proteolysis and traction force. The Journal of Cell Biology 201, 1069-1084 (2013).
- Heuzé, M. L., Collin, O., Terriac, E., Lennon-Dumenil, A.-M. & Piel, M. in Methods in Molecular Biology 769, 415-434 (Humana Press, 2011).
- Pankov, R. A Rac switch regulates random versus directionally persistent cell migration. The Journal of Cell Biology 170, 793-802 (2005).
- Dang, I. et al. Inhibitory signalling to the Arp2/3 complex steers cell migration. Nature 1-19 (2013). doi:10.1038/nature12611 · DOI
- Insall, R. H. Understanding eukaryotic chemotaxis: a pseudopod-centred view. 1-6 (2010). doi:10.1038/nrm2905 · DOI
- Le Berre, M., Zlotek-Zlotkiewicz, E., Bonazzi, D., Lautenschlaeger, F. & Piel, M. Methods forTwo-DimensionalCell Confinement. Methods in Cell Biology -Volume 97 121, 213-229 (Elsevier Inc., 2014).
- Small, J. V., Herzog, M. & Anderson, K. Actin filament organization in the fish keratocyte lamellipodium. The Journal of Cell Biology 129, 1275-1286 (1995).
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HEM1 Actin Immunodysregulatory Disorder: Genotypes, Phenotypes, and Future Directions
Cook, S., Lenardo, M. J., & Freeman, A. F. (2022) · Journal of Clinical Immunology · doi:10.1007/s10875-022-01327-0 · Cited by 24 · see citing works
- Authors
- Leithner, A., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., Merrin, J., de Gorter, D. J. J., Schur, F., Bayerl, J., de Vries, I., Wieser, S., Hauschild, R., Lai, F. P. L., Moser, M., Kerjaschki, D., Rottner, K., Small, J. V., Stradal, T. E. B., & Sixt, M.
- Affiliations
- Institute of Science and Technology Austria (AT)
- Institute of Molecular Biotechnology (AT)
- Helmholtz Centre for Infection Research (DE)
- Max Planck Institute of Biochemistry (DE)
- Medical University of Vienna (AT)
- University of Münster (DE)
- Corresponding author
- Leithner, Alexander
- Eichner, Alexander
- Sixt, Michael
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2016-10-24
- Volume
- 18
- Issue
- 11
- Pages
- 1253-1259
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2538282264
- Cited by
- 163
- References
- 1
- Citations by year
- 2026: 11 · 2025: 15 · 2024: 10 · 2023: 12 · 2022: 22 · 2021: 25 · 2020: 14 · 2019: 20 · 2018: 18 · 2017: 15 · 2016: 1
- FWCI
- 10.29
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-sa
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- HZI (Helmholtz Centre for Infection Research) (submittedVersion, cc-by-nc-sa)
- Max Planck Digital Library (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Institute of Science and Technology Austria
- Deutsche Forschungsgemeinschaft
- FP7 Ideas: European Research Council (281556)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Keywords
- actin protrusions, filopodia, lamellipodia, leukocyte migration, WAVE complex, Arp2/3 complex, actin filament branching, chemotaxis, directional persistence, cell shape, leading edge, environmental exploration
- MeSH terms
- Actins, Animals, Cell Movement, Dendritic Cells, Leukocytes, Actin Cytoskeleton, Pseudopodia, Mice, Knockout, Actin-Related Protein 2-3 Complex, Mice, Polymerization
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