Professor Will Wood
Immune cell migration during inflammation and Infection.
- Dr Andrew Davidson, Postdoctoral Researcher
- Dr Frederico Rodrigues, Postdoctoral Researcher
- Dr Anna Franz, Postdoctoral Researcher (shared with Professor Paul Martin, University of Bristol)
- Dr Kate Comber, Lab Manager
- Jennie Campbell, PhD student
Cell movement is an essential process during both embryonic development and throughout adult life. The failure of cells to migrate to their appropriate locations can result in severe abnormalities or disease. It is therefore vital that the mechanism controlling cell migration is fully understood.
My lab uses Drosophila embryonic blood cells (hemocytes) as a model to study cell migration and chemotaxis in the context of a living organism. Hemocytes are large, macrophage-like cells that patrol tissues, recognising and engulfing apoptotic corpses in the embryo and pathogens in the larval and adult fly. During embryonic development hemocytes leave their point of origin in the head mesoderm, and crawl along specified pathways to populate the entire embryo by late embryogenesis. This process is highly regulated and adheres to a developmental programme with cells always migrating along the same stereotypical pathways within the embryo. As well as undergoing these developmental migrations, embryonic hemocytes will also rapidly chemotax toward an epithelial wound in a process that closely resembles vertebrate inflammation. Additionally, these multi-tasking cells will engulf and clear bacteria at sites of infection as well as apoptotic corpses that arise as part of normal embryonic development.
Using confocal live imaging and the powerful methods of experimental genetics available in Drosophila we are uncovering the signals that guide hemocytes during each of their migrations and how these immune cells are able to prioritize different cues within the complex setting of a 3-dimensional organism. We are studying the nature and regulation of the actin protrusions observed in hemocytes and are interested in understanding the molecular mechanism by which these cells are able to sense and polarise toward an attractive source, be it a wound, an apoptotic corpse, or the presence of bacteria at a site of infection.
- Franz A, Wood W, Martin P. Fat body cells are motile and actively migrate to wounds to drive repair and prevent infection. Developmental Cell 2018; 44:460-470.
- Lin L, Rodrigues F, Kary C, Logan M, Baxter R, Wood W, Baehrecke E. Complement-related regulates autophagy in neighboring cells. Cell 2017; 170(1):158-171.
- Wood W, Martin P. Macrophage Functions in Tissue Patterning and Disease – New Insights from the Fly. Developmental Cell 2017; 40(3): 221-233.
- Weavers H, Evans I, Martin P, Wood W. Corpse engulfment generates a molecular memory that primes the macrophage inflammatory response. Cell 2016; 165(7): 1658-1671.
- Evans I, Rodrigues F, Armitage E, Wood W. Draper/CED1 mediates an ancient damage response to control inflammatory blood cell migration in vivo. Current Biology 2015; 25:1606-1612.
- Wellcome Trust Senior Research Fellowship
- MRC Programme Grant (jointly held with Professor Paul Martin, University of Bristol)
- Alzheimer’s Society Project Grant