Thuma, Leila, Carter, Deborah, Weavers, Helen and Martin, Paul ORCID: https://orcid.org/0000-0002-2665-5086 2018. Drosophilaimmune cells extravasate from vessels to wounds using Tre1 GPCR and Rho signaling. Journal of Cell Biology 217 (9) , pp. 3045-3056. 10.1083/jcb.201801013 |
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Abstract
Inflammation is pivotal to fight infection, clear debris, and orchestrate repair of injured tissues. Although Drosophila melanogaster have proven invaluable for studying extravascular recruitment of innate immune cells (hemocytes) to wounds, they have been somewhat neglected as viable models to investigate a key rate-limiting component of inflammation—that of immune cell extravasation across vessel walls—due to their open circulation. We have now identified a period during pupal development when wing hearts pulse hemolymph, including circulating hemocytes, through developing wing veins. Wounding near these vessels triggers local immune cell extravasation, enabling live imaging and correlative light-electron microscopy of these events in vivo. We show that RNAi knockdown of immune cell integrin blocks diapedesis, just as in vertebrates, and we uncover a novel role for Rho-like signaling through the GPCR Tre1, a gene previously implicated in the trans-epithelial migration of germ cells. We believe this new Drosophila model complements current murine models and provides new mechanistic insight into immune cell extravasation.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Additional Information: | This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/). |
Publisher: | Rockefeller University Press |
ISSN: | 0021-9525 |
Date of First Compliant Deposit: | 26 July 2018 |
Date of Acceptance: | 29 May 2018 |
Last Modified: | 03 May 2023 19:56 |
URI: | https://orca.cardiff.ac.uk/id/eprint/113461 |
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