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18 results on '"Millard, Tom H."'

1. The anomalous tango of hemocyte migration in Drosophila melanogaster embryos

Author

Korabel, Nickolay, Clemente, Giuliana D., Han, Daniel, Feldman, Felix, Millard, Tom H., and Waigh, Thomas Andrew

Subjects
Physics - Biological Physics, Condensed Matter - Statistical Mechanics, Quantitative Biology - Cell Behavior
Abstract

Drosophila melanogaster hemocytes are highly motile cells that are crucial for successful embryogenesis and have important roles in the organism's immunological response. Hemocyte motion was measured using selective plane illumination microscopy. Every hemocyte cell in one half of an embryo was tracked during embryogenesis and analysed using a deep learning neural network. The anomalous transport of the cells was well described by fractional Brownian motion that was heterogeneous in both time and space. Hemocyte motion became less persistent over time. LanB1 and SCAR mutants disrupted the collective cellular motion and reduced its persistence due to the modification of viscoelasticity and actin-based motility respectively. The anomalous motility of the hemocytes oscillated in time with alternating epoques of varying persistent motion. Touching hemocytes experience synchronised contact inhibition of locomotion; an anomalous tango. A quantitative statistical framework is presented for hemocyte motility which provides new biological insights., Comment: 13 pages, 7 figures

Published
2021

4. Activating RAC1 variants in the switch II region cause a developmental syndrome and alter neuronal morphology

Author

Banka, Siddharth, primary, Bennington, Abigail, additional, Baker, Martin J, additional, Rijckmans, Ellen, additional, Clemente, Giuliana D, additional, Ansor, Nurhuda Mohamad, additional, Sito, Hilary, additional, Prasad, Pritha, additional, Anyane-Yeboa, Kwame, additional, Badalato, Lauren, additional, Dimitrov, Boyan, additional, Fitzpatrick, David, additional, Hurst, Anna C E, additional, Jansen, Anna C, additional, Kelly, Melissa A, additional, Krantz, Ian, additional, Rieubland, Claudine, additional, Ross, Meredith, additional, Rudy, Natasha L, additional, Sanz, Javier, additional, Stouffs, Katrien, additional, Xu, Zhuo Luan, additional, Malliri, Angeliki, additional, Kazanietz, Marcelo G, additional, and Millard, Tom H, additional

Published
2022
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6. Ena orchestrates remodelling within the actin cytoskeleton to drive robust Drosophila macrophage chemotaxis

Author

Davidson, Andrew J, Millard, Tom H, Evans, Iwan R, and Wood, Will

Subjects
macromolecular substances
Abstract

The actin cytoskeleton is the engine that powers the inflammatory chemotaxis of immune cells to sites of tissue damage or infection. Here, we combine genetics with live in vivo imaging to investigate how cytoskeletal rearrangements drive macrophage recruitment to wounds in Drosophila. We find that the actin-regulatory protein Ena is a master regulator of lamellipodial dynamics in migrating macrophages, where it remodels the cytoskeleton to form linear filaments that can then be bundled together by the cross-linker Fascin (also known as Singed in flies). In contrast, the formin Dia generates rare, probing filopods for specialised functions that are not required for migration. The role of Ena in lamellipodial bundling is so fundamental that its overexpression increases bundling even in the absence of Fascin by marshalling the remaining cross-linking proteins to compensate. This reorganisation of the lamellipod generates cytoskeletal struts that push against the membrane to drive leading edge advancement and boost cell speed. Thus, Ena-mediated remodelling extracts the most from the cytoskeleton to power robust macrophage chemotaxis during their inflammatory recruitment to wounds.

Published
2019

7. Ena orchestrates remodelling within the actin cytoskeleton to drive robust Drosophila macrophage chemotaxis

Author

Davidson, Andrew J., Millard, Tom H., Evans, Iwan R., and Wood, Will

Subjects
Inflammation, Wound Healing, Macrophage, Chemotaxis, Macrophages, Microfilament Proteins, Short Report, Formins, Hemocyte, macromolecular substances, Ena, Animals, Genetically Modified, DNA-Binding Proteins, Actin Cytoskeleton, Multiprotein Complexes, Animals, Drosophila Proteins, Drosophila, Pseudopodia, Carrier Proteins, Actin, Migration, Protein Binding
Abstract

The actin cytoskeleton is the engine that powers the inflammatory chemotaxis of immune cells to sites of tissue damage or infection. Here, we combine genetics with live in vivo imaging to investigate how cytoskeletal rearrangements drive macrophage recruitment to wounds in Drosophila. We find that the actin-regulatory protein Ena is a master regulator of lamellipodial dynamics in migrating macrophages, where it remodels the cytoskeleton to form linear filaments that can then be bundled together by the cross-linker Fascin (also known as Singed in flies). In contrast, the formin Dia generates rare, probing filopods for specialised functions that are not required for migration. The role of Ena in lamellipodial bundling is so fundamental that its overexpression increases bundling even in the absence of Fascin by marshalling the remaining cross-linking proteins to compensate. This reorganisation of the lamellipod generates cytoskeletal struts that push against the membrane to drive leading edge advancement and boost cell speed. Thus, Ena-mediated remodelling extracts the most from the cytoskeleton to power robust macrophage chemotaxis during their inflammatory recruitment to wounds., Summary: Macrophages must migrate to a variety of stimuli, including inflammatory wounds. We identify the actin-regulatory protein Ena as a master remodeller of the cytoskeleton within migrating macrophages in vivo.

Published
2019

9. RAC1 Missense Mutations in Developmental Disorders with Diverse Phenotypes

Author

Reijnders, Margot R.F., primary, Ansor, Nurhuda M., additional, Kousi, Maria, additional, Yue, Wyatt W., additional, Tan, Perciliz L., additional, Clarkson, Katie, additional, Clayton-Smith, Jill, additional, Corning, Ken, additional, Jones, Julie R., additional, Lam, Wayne W.K., additional, Mancini, Grazia M.S., additional, Marcelis, Carlo, additional, Mohammed, Shehla, additional, Pfundt, Rolph, additional, Roifman, Maian, additional, Cohn, Ronald, additional, Chitayat, David, additional, Millard, Tom H., additional, Katsanis, Nicholas, additional, Brunner, Han G., additional, and Banka, Siddharth, additional

Published
2017
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18. Endocytosis-dependent coordination of multiple actin regulators is required for wound healing.

Author

Yutaka Matsubayashi, Coulson-Gilmer, Camilla, and Millard, Tom H.

Subjects
*ENDOCYTOSIS, *ACTIN research, *WOUND healing, *REGENERATION (Biology), *CELL physiology
Abstract

The ability to heal wounds efficiently is essential for life. After wounding of an epithelium, the cells bordering the wound form dynamic actin protrusions and/or a contractile actomyosin cable, and these actin structures drive wound closure. Despite their importance in wound healing, the molecular mechanisms that regulate the assembly of these actin structures at wound edges are not well understood. In this paper, using Drosophila melanogaster embryos, we demonstrate that Diaphanous, SCAR, and WASp play distinct but overlapping roles in regulating actin assembly during wound healing. Moreover, we show that endocytosis is essential for wound edge actin assembly and wound closure. We identify adherens junctions (AJs) as a key target of endocytosis during wound healing and propose that endocytic remodeling of AJs is required to form "signaling centers" along the wound edge that control actin assembly. We conclude that coordination of actin assembly, AJ remodeling, and membrane traffic is required for the construction of a motile leading edge during wound healing. [ABSTRACT FROM AUTHOR]

Published
2015
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