Research groups
Mark Jepson
Senior Research Fellow & Manager of the Cell Imaging Facility
+44 (0)117 33 12143 (tel)
+44 (0)117 33 12168 (fax)
m.a.jepson@bristol.ac.uk
Research
Molecular mechanisms of host-pathogen interactions.
The virulence of pathogenic bacteria relies on their ability to induce signals within
host cells to alter their behaviour. This can involve surface expression of proteins,
secretion of toxins or, in some of the most interesting examples, direct transfer of
proteins by bacteria into host cells. The molecular mechanisms underlying bacterial
modulation of host cells have yet to be fully defined. My group’s research focuses on the
molecular mechanisms underlying the cross-talk between pathogenic bacteria with epithelial
cells. Our work has principally focused on Salmonella and enteropathogenic E. coli (EPEC)
but newer projects have extended our research interests to encompass also Campylobacter,
Streptococci and EHEC. Specific areas of interest include: 1) understanding how bacteria
modulate the actin cytoskeleton and intracellular trafficking; 2) understanding how
bacteria alter epithelial permeability; 3) defining the role of particle-transporting
epithelial cells (M cells) in bacterial infection; 4) applying cell imaging techniques to
the study of microbial pathogenesis.
Confocal images of actin rearrangement induced during Salmonella infection of epithelial cells.
Group
Suzanne Humphrey, Layla Malt, Caryn Harward, Alan Leard, Katy Jepson.
Recent publications
Perrett CA & Jepson MA (2009) Regulation of Salmonella-induced membrane ruffling by SipA differs in strains lacking other effectors. Cellular Microbiology 11: 475-87.
Clark L, Martinez-Argudo I, Humphrey TJ & Jepson MA (2009) GFP plasmid induced defects in Salmonella invasion depend on plasmid architecture not protein expression. Microbiology 155: 461-7.
Perrett CA, Karavolos MH, Humphrey S, Mastroeni P, Martinez-Argudo I, Spencer H, Bulmer D, Winzer K, McGhie E, Koronakis V, Williams P, Khan CMA & Jepson MA (2009) LuxS-based quorum sensing does not affect the ability of Salmonella to express the SPI-1 Type 3 secretion system, induce membrane ruffles or invade epithelial cells. Journal of Bacteriology 191: 7253-9.
Berger CN, Crepin VF, Jepson MA, Arbeloa A & Frankel
G (2009) The mechanisms used by enteropathogenic Escherichia
coli to control filopodia dynamics. Cellular Microbiology 11: 309-322.