Forthcoming events in this series


Fri, 24 Jan 2014
14:00
L5

Spontaneous motility of actin-based cell fragments as a free-boundary problem

Prof Jaume Casademunt
(University of Barcelona)
Abstract

We show that actin lamellar fragments extracted from cells, lacking

the complex machinery for cell crawling, are spontaneously motile due

solely to actin polymerization forces at the boundary. The motility

mechanism is associated to a morphological instability similar to the

problem of viscous fingering in Hele-Shaw cells, and does not require

the existence of a global polarization of the actin gel, nor the

presence of molecular motors, contrary to previous claims. We base our

study on the formulation of a 2d free-boundary problem and exploit

conformal mapping and center manifold projection techniques to prove

the nonlinear instability of the center of mass, and to find an exact

and simple relation between shape and velocity. A complex subcritical

bifurcation scenario into traveling solutions is unfolded. With the

help of high-precision numerical computation we show that the velocity

is exponentially small close to the bifurcation points, implying a

non-adiabatic mechanism. Examples of traveling solutions and their

stability are studied numerically. Extensions of the approach to more

realistic descriptions of actual biological systems are briefly

discussed.

REF: C. Blanch-Mercader and J. Casademunt, Physical Review Letters

110, 078102 (2013)

Fri, 01 Nov 2013

14:00 - 15:00
L5

Design principles and dynamics in clocks, cell cycles and signals

Professor David Rand
(University of Warwick)
Abstract

I will discuss two topics. Firstly, coupling of the circadian clock and cell cycle in mammalian cells. Together with the labs of Franck Delaunay (Nice) and Bert van der Horst (Rotterdam) we have developed a pipeline involving experimental and mathematical tools that enables us to track through time the phase of the circadian clock and cell cycle in the same single cell and to extend this to whole lineages. We show that for mouse fibroblast cell cultures under natural conditions, the clock and cell cycle phase-lock in a 1:1 fashion. We show that certain perturbations knock this coupled system onto another periodic state, phase-locked but with a different winding number. We use this understanding to explain previous results. Thus our study unravels novel phase dynamics of 2 key mammalian biological oscillators. Secondly, I present a radical revision of the Nrf2 signalling system. Stress responsive signalling coordinated by Nrf2 provides an adaptive response for protection against toxic insults, oxidative stress and metabolic dysfunction. We discover that the system is an autonomous oscillator that regulates its target genes in a novel way.

Fri, 18 Oct 2013

14:00 - 15:00
L5

Exact representations of Susceptible-Infectious-Removed (SIR) epidemic dynamics on networks

Dr Kieran Sharkey
(University of Liverpool)
Abstract

The majority of epidemic models fall into two categories: 1) deterministic models represented by differential equations and 2) stochastic models which can be evaluated by simulation. In this presentation I will discuss the precise connection between these models. Until recently, exact correspondence was only established in situations exhibiting large degrees of symmetry or for infinite populations.

I will consider SIR dynamics on finite static contact networks. I will give an overview of two provably exact deterministic representations of the underlying stochastic model for tree-like networks. These are the message passing description of Karrer and Newman and my pair-based moment closure representation. I will discuss relationship between the two representations and the relative merits of both.

Fri, 13 Sep 2013

11:00 - 12:00
L4

STUDIES OF SINGLE CELL AND CELL POPULATION BEHAVIORS IN 3D CO-CULTURE MICROFLUIDIC SYSTEMS

Professor Roger Kamm
(Massachusetts Institute of Technology)
Abstract

Recent years have seen rapid expansion of the capabilities 
to recreate in vivo conditions using in vitro microfluidic assays.  
A wide range of single cell and cell population behaviors can now 
be replicated, controlled and imaged for detailed studies to gain 
new insights.  Such experiments also provide useful fodder for 
computational models, both in terms of estimating model parameters 
and for testing model-generated hypotheses.  Our experiments have 
focused in several different areas.  
1) Single cell migration experiments in 3D collagen gels have 
revealed that interstitial flow can lead to biased cell migration 
in the upstream direction, with important implications to cancer 
invasion.  We show this phenomenon to be a consequence of 
integrin-mediated mechanotransduction.  
2) Endothelial cells seeded in fibrin gels form perfusable 
vascular networks within 2-3 days through a process termed 
“vasculogenesis”.  The process by which cells sense their 
neighbours, extend projections and form anastomoses, and 
generate interconnected lumens can be observed through time-lapse 
microscopy.  
3) These vascular networks, once formed, can be perfused with 
medium containing cancer cells that become lodged in the 
smaller vessels and proceed to transmigrate across the endothelial 
barrier and invade into the surrounding matrix.  High resolution 
imaging of this process reveals a fascinating sequence of events 
involving interactions between a tumour cell, endothelial cells, 
and underlying matrix.  These three examples will be presented 
with a view toward gaining new insights through computational 
modelling of the associated phenomena.

Fri, 10 May 2013
14:00
L1

Mechanical models to explore biological phenomena

Dr Rachele Allena
(ENSAM)
Abstract

Mechanics plays an important role during several biological phenomena such as morphogenesis,

wound healing, bone remodeling and tumorogenesis. Each one of these events is triggered by specific

elementary cell deformations or movements that may involve single cells or populations of cells. In

order to better understand how cell behave and interact, especially during degenerative processes (i.e.

tumorogenesis and metastasis), it has become necessary to combine both numerical and experimental

approaches. Particularly, numerical models allow determining those parameters that are still very

difficult to experimentally measure such as strains and stresses.

During the last few years, I have developed new finite element models to simulate morphogenetic

movements in Drosophila embryo, limb morphogenesis, bone remodeling as well as single and

collective cell migration. The common feature of these models is the multiplicative decomposition of

the deformation gradient which has been used to take into account both the active and the passive

deformations undergone by the cells. I will show how this mechanical approach, firstly used in the

seventies by Lee and Mandel to describe large viscoelastic deformations, can actually be very

powerful in modeling the biological phenomena mentioned above.