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Professor Paul Martin

Professor Paul Martin

Professor Paul Martin
BSc(Sus), PhD(Lond)

Professor of Cell Biology

Professor of Cell Biology

Area of research

Inflammation in repair and cancer

Office F32
School of Medical Sciences,
University Walk, Clifton BS8 1TD
(See a map)

+44 (0) 117 331 2298


Embryos heal wounds very rapidly and efficiently and without leaving a scar. They appear to do this using a very similar portfolio of cellular tools to those used by embyos to undergo the natural morphogenetic movements of development. We hope that studying these parallels will help us better understand embryonic tissue movements and also suggest ways in which we might make adult tissues repair more efficiently. Using live confocal imaging of transgenic Drosophila embryos expressing gfp-actin in epithelial tissues we have compared repair of laser-generated epithelial wounds with the paradigm morphogenetic process of dorsal closure and show that remarkably similar actin-based actin machineries (an actomyosin pursestring and dynamic filopodia and lamellipodia) drive these two processes. It seems that very similar mechanisms may also be used by vertebrate embryos to zipper epithelial seams together, for example as the eyelids fuse during foetal development. We are currently interested in imaging the signalling episodes that direct the "starting" and "stopping" of these epithelial fusion and wound closure processes.

In adult mammalian skin wounds we see several hundred genes upregulated, many of these in the leading edge epidermal cells, and our recent studies indicate that a subset of these genes may first be epigenetically "unsilenced" by transient downregulation of the polycomb complex proteins and coincident upregulation of histone demethylases.

Scanning electron microscope view of a wound in a zebrafish larvae showing how contraction of the leading epithelial cells causes the wound margin to "scrunch-up" as it is drawn forward by the action of the actomyosin pursestring.

We have also become interested in the inflammatory response that is an inevitable consequence of any repair process in adult tissues. Our experiments in embryonic mice (where there is no inflammatory response), and in the neonatal PU.1 null mouse, which is genetically lacking the key leukocyte lineages, suggest that an inflammatory response is not essential for repair and may indeed be causal of fibrosis in post-embryonic animals. Consequently, we have used a microarray approach with this mouse in order to identify a portfolio of candidate inflammation/fibrosis genes and have begun to knock down each of these genes in turn to discover whether this might improve repair. When we knock down one of these inflammation-dependent genes, osteopontin, we find significantly improved healing without a scar. We have also established models of inflammation in the Drosophila embryo and in the translucent zebrafish larval tail fin, which allow us to make DIC movies of the inflammatory response and to dissect the genetics of inflammation, including the precise roles for each of the small GTPases and their effectors, in particular WASp, in recruitment of inflammatory cells to the wound site.

Most recently, we have used the translucent zebrafish larvae to compare the innate immune response to a wound and to "transformed" cells as they proliferate to form tumours in the skin. Our studies have shown that the same signal, H 2O 2, is the attractant in both situations and that immune cells impart some trophic signal(s) that encourage growth of transformed cells.


  • wound healing
  • metastasis
  • tumour formation

Selected publications

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Recent publications

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