Faculty of Biological Sciences

Faculty of Biological Sciences
Summer Vacation Studentship Opportunities 2017

Please Note that applications to this scheme have now closed

Are you interested in working in a Research Laboratory during the summer vacation?

We are offering the opportunity to work in a research laboratory during the summer vacation. This type of experience is ideal if you are thinking of continuing with a career in research after graduating, or if you would like to find out what research is all about.

Under these schemes the laboratories offer experimental projects in a wide variety of subject areas under the supervision of a postdoctoral research assistant and last up to 8 weeks. The stipends available are approximately £200 per week.

This year, the faculty will be supporting three different schemes, please see below for more information.

Eligible Students:

Science Students and Medical Students between the end of their second year and the end of their penultimate year (but not intercalating students).

Closing dates:

Dean's Studentships: 12 noon on Thursday 26th January

Jennifer Rowles Studenthsips: 12 noon on Thursday 26th January (Please note this scheme is only open to University of Leeds students)

Faculty Studentships: 12 noon on Thursday 26th January

Applications Procedure:

Please send your application by email, selecting 1 or 2 projects in order of preference.

If applying before January 27th, please email Lily Aarons at L.Aarons@leeds.ac.uk

If applying after January 27th, please email Liz Liversedge at E.Liversedge@leeds.ac.uk

Please note that you are able to apply for more than one scheme.

Students are chosen for Studentships by competition, so your application should consist of a curriculum vitae and letter including;

  • The title(s) of the the project(s) you are interested in. You may apply for more than one project, but please list in order of preference
  • Your school and university courses and grades to date
  • A statement of your career aims and how you might benefit from a Scholarship
  • The name, address, phone number and email addresses of two referees, preferably your tutors

Dean's Vacation Projects


Project Leader

Project Details

Dr Niluka Goonawardane

Unravelling the molecular basis of strain-specific Tick-borne encephalitis virus pathogenicity

The project is focussed on developing the tools to understand the strain-specific disease outcomes of Tick-borne encephalitis virus (TBEV). Tick-borne encephalitis (TBE) is a dangerous neuroinfection caused by TBEV that develops following the bite of an infected tick. TBEV belongs to a family of RNA viruses called Flaviviridae, which also includes Zika and Dengue virus. It is recognised that TBEV produces different clinical manifestations in humans but the reasons have never been elucidated at the molecular level and are the objectives of this research project.

This is a laboratory focused role, where you will conduct a specified programme of research supported by research training and guidance under the direct supervision of the Research Fellow. The project is based on the genetic engineering of TBEV replicon system, with designated properties, to identify both host and virus proteins and virus RNA dynamics through its life cycle as important molecular determinants of virus Pathogenic characteristics. You will be based in the laboratory of Prof. Mark Harris at the University of Leeds and work in an interactive and collaborative environment. You should have a good understanding of Molecular Biology, Cell Biology or a related discipline. Experience in cloning, tissue culture, and background in virology is a plus, but not required.

Dr Steven Harborne

Producing an improved strain of E. coli for membrane protein production

You will use molecular cloning, E. coli transformation and culture, and site-directed mutagenesis using PCR. You will also learn key protein chemistry such as purification, biophysical characterisation and structural biology.

We are working to try and stop Acridine resistance subunit B (AcrB), which is part of the AcrAB-TolC multi-protein complex (a multi-drug efflux pump of gram-negative bacteria), from binding to nickel sepharose resin. The problem is that E. coli AcrB is naturally histidine-rich, meaning that it is a common contaminant in the purification of recombinantly expressed, histidine-tagged membrane protein. AcrB crystallises very easily, whereas most other interesting membrane targets do not. Therefore, having small amounts of AcrB contamination in our samples causes false positive hits in crystallisation screening: a significant hindrance to the determination of new membrane protein structures.

You will be responsible for creating an AcrB construct that can no longer bind to nickel sepharose resin by replacing key histidine residues with alanine. This improved AcrB will then replace the native AcrB in E. coli, creating a vital tool for the recombinant expression of membrane proteins for crystallography.

The key objectives are:

  • Replace key His residues with Ala in AcrB
  • Test the mutant AcrB for binding to nickel resin
  • Replace native E. coli AcrB with improved AcrB in a number of expression strains
  • Test the growth of E. coli strains containing the improved AcrB protein
Dr Hannah Kirton

The role of Epac in cardiac function

A summer undergraduate studentship position is available for 8 weeks to investigate the role of Epac (exchange proteins directly activated by cyclic-AMP) in cardiac function. Epac are guanine nucleotide exchange factors for the small GTPase Rap1 and recently discovered as a novel, yet distinct, direct effector of cAMP, responsible for transmitting signals within the heart. Both Epac1 and Epac2 are expressed in the heart; however it is still unclear how expression levels in the heart change under physio and pathological conditions.

Current evidence suggests Epac-Rap1 inhibition plays a key role in cancer and cardiovascular therapeutics. However, limited evidence suggests impaired Epac-Rap1 signalling adversely affects cardiac function, including long QT interval and arrhythmia susceptibility. Thus far our lab has evidenced that selective Epac2 inhibition in rat ventricular myocytes is accompanied by the generation of early after depolarisation arrhythmias, due to elevated reactive oxygen species (ROS) generation, which subsequently activates the late Na current (INalate) and action potential prolongation. We, however, also believe Epac1 may be a key player in cardiac function. To identify the role and function of Epac1, relative to Epac2, we aim to localise their expression and expression levels in both control and disease-like states in rat ventricular myocytes.

You will work within the School of Biomedical Sciences, Cellular Cardiology laboratory (lead by Prof. D.S Steele) under the supervision of Dr H. M. Kirton at the Faculty of Biological Sciences. The project will utilise western blotting methods and interpret them to better understand modifications of Epac1 and Epac2 expression levels in rat ventricular myocytes. If time permits, this data may be complimented with immunocytochemistry.
Applicants should have research/laboratory experience. You should be enthusiastic and committed to working within the ethos of the laboratory, and to deliver exceptional data quality. You should have good communication and interpersonal skills. You will have good attention to detail, and willingness to attempt to critically analyse and assess results and techniques used.

Dr Sylvain Gigout

Alteration in expression of perineuronal nets (PNNs) during the development of epilepsy

PNNs are a pericellular aggregated extracellular matrix structure that are composed of a variety of proteoglycans and glycoproteins. PNNs are known to surround neuronal subpopulations throughout the CNS and play a key role in the termination of developmental plasticity (Kwok et al., 2011). We have previously demonstrated that removal of PNNs in the central nervous system enhances plasticity.


Epilepsy, as well as several other pathologies, display abnormal plasticity. For example, in absence epilepsy, changes in the excitation/inhibition balance in the thalamocortical network have been observed. This type of generalised epilepsy involves both the thalamus and the cortex. Therefore, it is proposed that changes to normal PNNs expression in these brain areas may explain the alteration in thalamocortical excitability.


This project will investigate if PNN expression is affected during the course of epilepsy, by using a genetic model, the GAERS (Genetic Absence Epilepsy Rat from Strasbourg; see Danober et al., 1998 for a review). You will work within the School of Biomedical Sciences, Leeds Group for Spinal Cord Injury Research (PNN lab; led by Dr Jessica Kwok) under the supervision of Dr S. Gigout at the Faculty of Biological Sciences. The project will utilise cryoprotected slices of rat brain with immunohistochemistry and confocal imaging. The candidate will interpret these data to better understand modifications of PNN components expression levels in rat brain.


Applicants should be enthusiastic and committed to working within the ethos of the laboratory, and to deliver exceptional data quality. Willingness to attempt to critically analyse and assess results and techniques used, as well as a good attention to detail, are essential.


Jennifer Rowles Projects:


Project Leader

Project Details

Dr Ian Wood

Therapeutic potential of HDAC inhibitors for multiple sclerosis.

Recently, inhibitors of histone deacetylase enzymes (HDACi) have been identified as having potential therapeutic value for a range of neuronal disorders including multiple sclerosis and other neurodegenerative diseases [1, 2]. The HDACis have been shown to have neuroprotective and anti-inflammatory properties yet their mechanism of action remains unidentified. Progress in our understanding has been further hampered because there are 18 known HDAC enzymes and the specific contribution of each HDAC to disease states has not been elucidated. One reason for the lack of progress is that the available HDACis lack selectivity for specific HDACs precluding identification of individual HDACs by pharmacological approaches. The University of Leeds has produced novel HDAC inhibitors that we have shown have neuroprotective properties [3] and act as anti-inflammatory agents. This project will use our novel HDAC inhibitors as well as commercially available inhibitors to characterise the effects of HDACis on the inflammatory response of microglial cells. The approach will involve the use of cell culture methods, functional assays to quantify cell responses such as proliferation as well as molecular approaches to quantify cytokine production and changes in gene expression.

1. Konsoula, Z. and F.A. Barile, Epigenetic histone acetylation and deacetylation mechanisms in experimental models of neurodegenerative disorders. J Pharmacol Toxicol Methods, 2012. 66(3): p. 215-20.

2. Faraco, G., L. Cavone, and A. Chiarugi, The therapeutic potential of HDAC inhibitors in the treatment of multiple sclerosis. Mol Med, 2011. 17(5-6): p. 442-7.

3. Durham, B., Novel histone deacetylase (HDAC) inhibitors with improved selectivity for HDAC2 and 3 protect against neural cell death. Bioscience Horizons, 2012. 5.

Dr Jonathan Lippiat

Axonal Kv1 channels as targets for multiple sclerosis pharmacotherapy

Fampridine (4-aminopyridine) has demonstrable clinical efficacy in relieving symptoms of multiple sclerosis. They inhibit voltage-dependent potassium channels in axons to improve action potential conduction, but in a non-specific manner. They therefore have many unwanted and toxic effects, which limit their use.  The aim of this project is to study the structure, function, and pharmacology of Kv1 channels that have a subunit arrangement consistent with axonal expression. The experimental approach will be to generate mammalian expression constructs encoding cloned human Kv1.1 and Kv1.2 channel subunits, fused together in specific orders. Expression systems will be generated and analysed using functional assays such as electrophysiology and/or fluorescence. One objective will be to generate a strategy for purifying channel complexes for structural studies using electron microscopy.

Starting reference:

Judge & Bever (2006) Potassium channel blockers in multiple sclerosis: neuronal Kv channels and effects of symptomatic treatment. Pharmacol Ther 111:224-59.

Professor Jim Deuchars

Identifying and modulating production of new cells in the spinal cord

We have recently discovered that we can use particular chemicals to induce or reduce the production of new cells in the spinal cord. In the long term we hope to harness this neurogenesis to repair conditions in which the spinal cord malfunctions, such as in spinal cord injury, motor neuron diseases or multiple sclerosis. This project will investigate the effects of particular treatments on neurogliogenesis in the spinal cord, aiming to convert the new cells to neurones and/or glia.

Techniques: Tissue culture, immunohistochemistry, confocal microscopy, histological tissue sectioning



Faculty Vacation Projects


Project Leader

Project Details

Dr Beatrice Filippi

How increase in iNOS levels affects insulin sensitivity in the Dorsal Vagal Complex.

We study the molecular mechanisms responsible for insulin resistance in the brain. The Dorsal Vagal Complex in the brainstem senses increases in circulating insulin levels and triggers a neuronal relay to the liver to decrease glucose production and blood glucose levels in rodents. Rodents become insulin resistant when fed with a high fat diet and the DVC fails to sense insulin and regulate blood glucose levels. Our aim is to understand the signaling events that trigger the loss of insulin sensitivity.

One of the potential events that can trigger insulin resistance is the increase in iNOS levels that leads to an increase in nitrosylated proteins. For this summer project the student will be involved in developing an adenovirus that expresses shRNA for iNOS in order to knock down this protein in the DVC. This adenovirus will then be injected into the DVC of rats via a double cannula inserted during a brain surgery. This will allow us to specifically knock down iNOS in the DVC and to look at the effect on insulin-dependent glucose regulation.

The student will learn how to design and clone the adenovirus. In addition he/she will be involved in testing the virus in vitro (in cells) and in vivo (animals).

Dr Emanuele Paci

Project 1

The student will use models and computer simulations to interpret experimental measurements for protein that is unfolded but interacts with partners. 

NMR data includes NOEs and paramagnetic relaxation enhancement (PRE) measurements. No previous knowledge of computers is required, but interest in learning about computational methods and how these can provide an interpretation of structural biophysical data.

Dr Emanuele Paci

Project 2

Sparse experimental data can be used to assess the relation of structural models and experiments. The project will consist in contributing to the development of a computer code that uses a genetic algorithm to select, among a broad set of structures generated through simulation or ab initio modelling programmes (e.g., Rosetta), structures consistent with heterogeneous experimental data (NMR, MS, CryoEM, SAXS,…). Some previous knowledge of computers (Linux) and programming languages (e.g. python, C) is required.

Professor Stuart Egginton

Extreme cardiovascular physiology – explaining cardiac function in severely dilated hearts

A major problem in cardiovascular science is understanding how to cope with enlarged hearts as a result of disease that inevitably results in compromised function, sometimes fatally e.g. dilated cardiomyopathy (DCM, affects 1 in 250 people). Potential mechanisms to counteract chamber dilation and still preserve adequate cardiac output include adjustments in proteins associated with sarcomere structure. One of the most important of these, titin, constitutes about 10% of muscle mass, and is the third most abundant protein after actin and myosin. Titin errors are the commonest cause of DCM (~25% of cases) with damaging mutations mainly in the A-band region, indicating a compromised interaction with myosin.

This project offers a student the opportunity to work in one of the world’s leading labs examining how molecular structure defines muscle function (http://www.fbs.leeds.ac.uk/staff/profile.php?tag=Trinick), using cardiac samples from a unique groups of animals lacking respiratory pigment expression (http://www.fbs.leeds.ac.uk/staff/profile.php?tag=Egginton_S).  These icefishes have a ventricle size approximately 4 times that of related species, and are capable of generating huge stroke volumes. How this is achieved is a mystery. We will examine the titin content of these fishes and attempt to understand the highly unusual capacity for force development at high volumes, exploring whether or not this elastic component is essential for white hearts to function effectively.

The student will experience analytical protein chemistry by means of separation, electrophoresis and antibody selection, and correlate findings with recent data on in situ function of these amazing hearts, obtained for the first time on an Antarctic fieldtrip last year.