Monthly Seminar Program
Guest Speakers:
Dr. John Ward
Research Fellow Speaker:
Dr. Wayne Croft
Phd Speakers:
Eva Caamaño
Kathryn Richardson
Paddy Slator
1st March 2013
Seminar program
Time
13:00-14:00
Session
Lunch
Location
Common room
14:00-15:00
John Ward
MOAC Seminar room
15:00-15:15
Tea and co↵ee break
Common room
15:15-16:15
3 Phd Presentations
Phd presentations consist 15 minute talks (including questions) audience rotates between
three rooms
Eva Caamaño
Kathryn Richardson
Paddy Slator
MOAC Seminar Room
WSB 32
WSB 336
16:15-16:20
Break
Common room
16:20-16:45
Wayne Croft
MOAC Seminar room
16:45 onwards
Wine and Cheese
Common room
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Presentation Description
Guest Speaker Session
JOHN WARD
Quorum sensing
Dr. John Ward research interest lie the application of mathematical
modelling to problems in biology and medicine. This talk will focus on quorum sensing. More information about Dr Ward’s research interests including
a list of publications can be found at:
http://homepages.lboro.ac.uk/ majpw2/
Research Fellow Session
WAYNE CROFT
Oscillatory dynamics of Cdc42 for polarised cell growth.
A fundamental problem in cell biology is how cells determine discrete
sites for growth. The capability to polarise (form asymmetric shape and/or
asymmetrically distribute proteins/functions) is an absolute requirement for
most cell-types. Cell polarity is essential for development and maintenance
of tissue integrity, loss of polarity is considered a hallmark and precondition for human cancer, and its dysregulation can cause tumour cell invasion
into neighbouring tissues. Uncovering the molecular mechanisms that enable cells to polarise, define specific growth sites and to migrate is vitally
important for the development of innovative treatments to cell polarity related diseases. The highly conserved Rho-like GTPase Cdc42 is a central
player coordinating the actin cytoskeleton for polarised cell growth. We
utilise time-lapse fluorescence microscopy, quantitative image analysis and
kinetic computational modelling to investigate mechanisms regulating the
spatio-temporal activity of Cdc42 in determining cell growth sites. Recycling of a Ras protein upstream of Cdc42 is shown to be required for Cdc42
oscillations and subsequent bipolar cell growth in fission yeast.
Phd Session 1:
EVA CAAMAÑO
Systems biology, metabolic modelling and metabolomics of the
malaria parasite.
Malaria is a vector-borne infectious disease whose pathology and symptoms are caused by a protozoan parasite of the genus Plasmodium to whose
vector is the female mosquito of the genus Anopheles. Malaria is one of
the biggest killers in the world. In 2009, 225 million cases were reported,
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resulting in over half a million deaths. Unfortunately, no e↵ective vaccine
is available and, although there are e↵ective medications to both treat and
prevent malaria, resistance has developed to several of them. This resistance
is an increasing concern and emphasize the need for an economically viable
long-term treatment not susceptible to reduce its e↵ect.
Plasmodium has a complex life cycle with di↵erent stages. Despite all
the published knowledge about the parasite such as the genome sequence in
2002 or the metabolic models by Plata et al. and Huthmacher et al., there
are still big questions about the metabolic make up of the parasite. Understanding how the metabolism of Plasmodium works, where the drugs act and
how likely are these targets, to be replaced in the metabolism creating resistance, is of paramount importance in order to find new unique targets with
low probability of being tricked by the parasite. The aim of my PhD research
is to take a systems approach integrated with metabolomics and metabolic
modelling to create a metabolic network model for P. falciparum (the most
deadly among the genus). The novelty of this PhD includes the availability
of specific quantitative metabolic data that will allow the creation of a biologically qualitative and quantitative accurate model. Metabolome readouts
from parasites collected in response to drug perturbations will be included in
the modeling to evaluate the model and enhance its predictive power. This
approach will allow us to identify key nodes of regulation and determine how
metabolism responds to changes in the environment/drug perturbation.
Phd Session 2:
KATHRYN RICHARDSON
Desensitisation mechanisms of GPCR signalling pathways.
A chalk talk introducing GPCRs, yeast, yeast genetics and desensitisation mechanisms.
Phd Session 3:
PADDY SLATOR
Characterising cell membrane heterogeneity through analysis of
particle trajectories.
The organisation of the plasma membrane is complex. It is clear that
there is heterogenous structure which mediates functionality and a↵ects the
2D di↵usion of biomolecules. Single particle tracking and STED-FCS microscopy allow direct observation of the behaviour of single proteins and
lipids within the membrane (Eggeling et al., Sahl et al.). My project aims
to robustly interpret this data.
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