Dr Clare Muir
I graduated from the University of Edinburgh in 2011 and subsequently volunteered overseas as a veterinarian before working in small animal critical care.
I then joined a 4 year specialty training programme in veterinary anatomic pathology at the Royal Veterinary College, London, and Bridge Pathology, Bristol and qualified as a veterinary anatomic pathologist in 2018.
Throughout my career, I have always found research key to answering questions posed by my clinical work and I am now funded by a 4ward North Clinical Research Fellowship to investigate how bacteria avoid destruction inside immune cells.
In addition to my research, I am also Education Co-Coordinator for the British Society of Veterinary Pathologists.
How does the interplay of phosphatidylinositol lipids at the phagosomal membrane co-ordinate pathogen killing?
Brief summary of PhD project
Animals (including humans) are protected from bacterial infection by patrolling innate immune cells. Neutrophils (the most abundant phagocytes) engulf their prey into membrane-bound phagosomes, enabling targeted, segregated and highly concentrated microbicidal activity.
Phosphatidylinositol (PI) lipids dynamically change at the phagosomal membrane to facilitate pathogen killing. However, the exact mechanisms which control PI formation and the extent to which pathogens subvert this process have not been determined.
PI signalling is an emerging target to modulate host immune responses therapeutically, hence determining the precise role(s) of PI signalling in pathogen execution is a priority.
- Prof Stephen Renshaw (University of Sheffield)
- Prof Alison Condliffe (University of Sheffield)
Progress so far
Using transgenic zebrafish and high resolution confocal and Selective Plane Illumination Microscopy, I have developed a model to observe phagosome membrane dynamics in vivo.
This has enabled me to characterise dynamic lipid changes in real time.
I am also developing new transgenic zebrafish lines which will report a range of PI lipids and help me to study host killing mechanisms.