The London Research Institute research groups are based at Lincoln’s Inn Fields and Clare Hall. Our major research themes are: the biology of tumours and tissues, cellular regulatory mechanisms and genomic integrity and cell cycle.
Michael Way : Cell Motility
Goals
Previous and current research
The spatial and temporal regulation of cell adhesion and motility is essential during development and throughout the lifetime of multicellular organisms. Consequently, defects in cell adhesion and migration can be devastating, causing tumour cells to metastasise to distant parts of the body and establish new tumours. Understanding the molecular basis of signalling networks and their role in regulating the complex processes of cell adhesion and migration represents a formidable task. The work in my lab is aimed at unravelling this problem using a multidisciplinary approach, involving the latest imaging, biochemical and genetic approaches in a variety of systems. This includes the use of vaccinia virus as a model for both actin- and microtubule-based motility.
Future projects
1. Characterisation of the regulation and dynamics of virus-induced signalling cascades and actin-based motility.
2. Analysis of the role of Rho-GTPases in vaccinia-induced cell motility and morphogenesis.
3. Identification of protein complexes required for the microtubule-dependent motility of vaccinia and the establishment of in vitro viral motility assays.
4. Characterisation of the cellular role of Tes, a putative tumour suppressor.
Selected Papers
Boeda B, Knowles PP, Briggs D, Murray-Rust J, Soriano E, Garvalov BK, McDonald NQ, Way M. Molecular recognition of the Tes LIM2-3 domains by the actin-related protein Arp7A. J Biol Chem. 2011;286:11543-11554
(Abstract)
Dodding MP, Mitter R, Humphries AC, Way M. A Kinesin-1 binding motif in vaccinia virus that is widespread throughout the human genome. EMBO J. 2011;30: 4523-4538.
(Abstract)
Dodding MP, Way M. Coupling viruses to dynein and kinesin-1. EMBO J. 2011;30:3527-3539
(Abstract)
Dodding MP, Way M. Nck- and N-WASP-dependent actin-based motility is conserved in divergent vertebrate poxviruses. Cell Host and Microbe. 2009;6:536-550.
(Abstract)
Weisswange I, Newsome TP, Schleich S, Way M. The rate of N-WASP exchange limits the extent of Arp2/3 complex dependent actin–based motility. Nature. 2009;458:87-91
(Abstract)
Arakawa Y, Cordeiro JV, Schleich S, Newsome TP, Way M. The release of vaccinia virus from infected cells requires RhoA-mDia modulation of cortical actin. Cell Host and Microbe. 2007;1:227-240
(Abstract)
Boëda B, Briggs DC, Higgins T, Garvalov BK, Fadden AJ, McDonald NQ, Way M. Tes, a specific Mena interacting partner, breaks the rules for EVH1 binding. Molecular Cell. 2007;28:1071-1082
(Abstract)
Greber U, Way M. A super highway to virus infection. Cell. 2006;174:741-754
(Abstract)
Valderrama F, Cordeiro JV, Schleich S, Frischknecht F, Way M. Vaccinia virus induced cell motility requires F11L-mediated inhibition of RhoA signalling. Science. 2006;311:377-381
(Abstract)
Newsome TP, Scaplehorn N, Way M. Src mediates a switch from microtubule to actin-based motility of vaccinia virus. Science. 2004;306:124-129
(Abstract)
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Michael Way
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