Judy Armitage – Getting to where you want to be: bacterial swimming and its
control
Bacteria swim by rotating semi-rigid helical flagellar filaments, using an ion
driven rotary motor embedded in the membrane. Bacteria are too small to sense
a spatial gradient and therefore sense changes in time, and use the signals to
bias their direction changing pattern to bias overall swimming towards a
favourable environment. I will discuss how interdisciplinary research has
helped us understand both the mechanism of motor function and its control by
chemosensory signals.

Oreste Acuto – Modelling T cell antigen receptor signalling
T cells stimulation by antigen (peptide-MHC, pMHC) initiates adaptive
immunity, a major factor contributing to vertebrate fitness. The T cell
antigen receptor (TCR) present on the surface of T cells is the critical
sensor for the recognition of and response to “foreign” entities, including
microbial pathogens and transformed cells. Much is known about the complex
molecular machine physically connected to the TCR to initiate, propagate and
regulate signals required for cellular activation. However, we largely ignore
the physical distribution, dynamics and reaction energetics of this machine
before and after TCR binding to pMHC. I will illustrate a few basic notions of
TCR signalling and potent quantitative in-cell approaches used to interpret
TCR signalling behaviour. I will provide two examples where mathematical
formalisation will be welcome to better understand the TCR signalling process.

David Vaux – Amyloid hydrogels: Pathogenic structures with similarity to
cellular gel phases
A wide range of chronic degenerative diseases of mankind result from the
accumulation of altered forms of self proteins, resulting in cell toxicity,
tissue destruction and chronic inflammatory processes in which the body’s
immune system contributes to further cell death and loss of function. A
hallmark of these conditions, which include major disease burdens such as
Alzheimer’s Disease and type II diabetes, is the formation of long fibrillar
polymers that are deposited in expanding tangled masses called plaques.
Recently, similarities between these pathological accumulations and
physiological mechanisms for organising intracellular space have been
recognised, and formal demonstrations that amyloid accumulations form
hydrogels have confirmed this link. We are interested in the pathological
consequences of amyloid hydrogel formation and in order to study these
processes we combine modelling of the assembly process with biophysical
measurement of gelation and its cellular consequences.