Undergraduate summer studentships

2025 scheme now open

The deadline for applications is Thursday 6^th February 2025 at 5pm.  Please send your application via email to fbsbusiness@leeds.ac.uk.  Applications should consist of a covering letter and your curriculum vitae.  Please note that a maximum of two projects can be applied for.  If you are applying for two projects, please ensure you state your order of preference.

These projects are offered by Faculty postdocs and are internally funded.  Once you have applied, if your application is shortlisted, you will be invited to attend an interview.  Successful candidates will be supervised in the lab by the postdoc leading the project. 

The stipend offered to the undergraduate is £270 per week.

Find out more about our projects below.

Dr Silvia Caggiari: Evaluating modulations in biomechanical and viscoelastic muscle properties following leg cycling: can these inform onset of fatigue?

For more details about the placement and information on how to apply, please read the job description

Individuals with spinal cord injury (SCI) present with a range of motor and sensory deficits, with spasticity representing a common complication, causing stiffness, muscle spasms and fatigue and limiting their involvement in rehabilitation. Rehabilitation after a SCI is complex and establishing effective and personalised strategies remains a challenge. Leg cycling represents a common intervention, which has been demonstrated to reduce spastic muscle tone when combined with electrical stimulation (ES)1, which represents a common adjunct therapy. Evaluating muscle properties is difficult, with clinically used assessments e.g. Modified Ashworth Scale, subjective and non-repeatable in nature. By contrast, objective measurements (surface electromyography) require expensive equipment.

Evaluating muscle properties e.g. stiffness, tone, mechanical relaxation has become frequently used in many clinical situations2, and this has been demonstrated in a SCI population3. However, no data are available to evaluate these modulations following rehabilitation interventions e.g., leg cycling, and their relationship with rehabilitation-induced fatigue.

This motivated the proposed project which aims at evaluating whether modulations in biomechanical and viscoelastic muscle properties can represent early predictors of induced fatigue, following combination of leg cycling and ES. This has the potential to inform rehabilitation interventions for people with SCI.

References: 1Thomaz,2019, 2McGowen,2023, 3Ge,2020

The successful student will join the ‘Motor Control and Neurorehabilitation’ research theme within the Cardiovascular and Exercise Science group, under the supervision of Dr Silvia Caggiari.

Ten healthy volunteers will be recruited from the local university community, under institutional ethics. They will undergo two separate sessions (performed on different days with >1 day wash-out in between) of 30-min incremental test (5-min stages 20W increments from 20 to 120W) with a cycle-ergometer, without and with transcutaneous electrical stimulation. Muscle properties will be recorded pre, during and post each session.

Objectives

Become familiarised with:

• Research protocol, participant information sheet, risk assessment (week 1).

• Use of specialist equipment (weeks 1 and 2).

• Data generated and their interpretation (weeks 1 and 2).

Lead participants recruitment and testing sessions (weeks 3, 4 and 5). This will involve:

• Ensure participants meet the eligibility criteria.

• Schedule the testing sessions.

• Collect and store consent forms and anthropometric data.

• Data collection.

Analysis and interpretation of the data (week 6 and 7)

Discuss and present the findings to the research group (week 8)

Dr Nitika Gupta – Identifying novel pain receptors in the sensory nervous system

For more details about the placement and how to apply, please read the job description

Somatosensation is the process by which we detect environmental and internal cues such as touch, changes in temperature, and body position. These stimuli can range from innocuous to painful, and in certain circumstances can cause tissue damage, so this process is crucial in order to determine our responses to changes in environment, maintain homeostasis and prevent injury. However, there are significant gaps in our understanding of the molecular mechanisms responsible, with growing evidence of currently unknown receptors yet to be discovered. Our aim is to develop a high-throughput screening approach to find these new targets using a combination of random mutagenesis with single-cell screening and fluorescent activated cell sorting (FACS). This allows us to generate a library of cells that respond to the stimulus of interest through the expression of a random selection of genes, and label them for downstream phenotypic, genotypic and transcriptomic analysis to identify the genes responsible. The discovery of novel sensory receptors through this approach could have major implications for understanding the causes of, and designing treatments for, conditions such as chronic pain and hypersensitivity.

Our current methodology to label stimulus-responsive cells from our high-throughput library relies on calcium indicators and therefore is dependent on the assumption that the stimulus of interest (e.g. temperature change) is activating a calcium signalling pathway. However, this may not capture other mechanisms that do not cause increases in intracellular calcium, such as voltage-dependent channels and pathways. This is particularly relevant in sensory neurons, which are electrically excitable and voltage sensing is key to their function. The project aims to tackle this problem by designing a novel system to identify and label cells where voltage-dependent, in addition to calcium-dependent, processes are activated in response to our stimulus of interest. This will involve using advanced molecular biology techniques to design, synthesise and isolate DNA constructs. Following this, a combination of tissue culture, cell transfection and FACS will be utilised to generate a cell line stably expressing this voltage and calcium reporting system, which can then be used in subsequent library screenings to identify novel sensory mechanisms.

Dr Joshua Jenkins – In situ architecture of Alzheimer’s disease-associated pathology

For more details about the placement and how to apply, please read the job description

The formation of filamentous amyloid proteins in the brain is a hallmark of many neurodegenerative diseases (e.g. Alzheimer’s and Parkinson’s disease). Cryo-electron microscopy (cryo-EM) has shown that amyloid filaments have disease-specific structures, indicating a link between structure and dysfunction. However, precisely how amyloid interacts with surrounding cellular components is still unknown. The next revolution in structural biology is to obtain structures of proteins within a native cellular and tissue context. Our team has made recent progress toward this goal, developing a correlative light and electron microscopy workflow to reveal the structure and organisation of amyloid filaments in post-mortem Alzheimer’s brain tissue. This approach enables us to explore the relationship between molecular and cellular pathology in neurodegeneration for the first time.

During your studentship you will receive training in computational processing of cryo-electron tomography (cryo-ET) datasets, including how to generate detailed three-dimensional reconstructions of cells and tissues for data annotation, segmentation and particle picking for subtomogram averaging. There will also be the opportunity to gain experience in cryo-ET sample preparation methods (e.g. high pressure freezing and cryo-fluorescence microscopy) and data collection (e.g. setting up tilt-series on the Titan Krios microscope).

Dr Hayley Pearson – COPs and robbers: hijacking the COPI complex during Bunyavirus infection

Bunyaviruses are a group of so-called ‘emerging’ viruses that infect humans causing fatal diseases including haemorrhagic fevers. As a measure of their threat, 3 of the 8 ‘priority’ viruses listed by the World Health Organisation are members of this Bunyavirus group, due to the lack of any vaccines or therapies. Our research focusses on uncovering novel host cell factors that are essential for Bunyavirus infection, which may be used as potential therapeutic targets.

One such cellular factor is a protein called COPI, which is involved in transport of proteins between compartments within cells. Our previous published work shows that three Bunyaviruses, lymphocytic choriomeningitis virus (LCMV), Hazara virus (HAZV) and Bunyamwera virus (BUNV) all require COPI for their replication (Fuller et al., 2020, DOI: 10.1128/JVI.00766-20; Byford et al., 2024, DOI: 10.1128/jvi.02006-23), raising the possibility that COPI complexes are required by all Bunyaviruses. Based on the native role of COPI, we hypothesize that Bunyaviruses need COPI to traffic newly-made infectious particles out of the infected cell. The studentship project is designed to test this hypothesis, by identifying the stage of the Bunyavirus infectious cycle that is blocked when COPI function is disrupted by using both gene silencing and pharmacological inhibition.

The objective of this project is to use BUNV as a model virus to further probe the role of COPI during Bunyavirus infection. Using virological assays that are well established in our lab, we firstly aim to test the three key stages of infection: virus entry, viral genome replication, and virus assembly and egress. We will use small molecule inhibitors to block the activity of the COPI components within cells at critical time points post-infection. Then, by using techniques such as western blotting, RT-qPCR, and wide field fluorescence microscopy, we will assess the effect of these inhibitors on each key event during the infectious cycle.

Our second aim is to reveal any interactions of the COPI components with viral proteins during BUNV infection. This will be achieved initially through visualisation of these components during infection by immunofluorescence and confocal microscopy analysis. We will further validate our findings by performing co-immunoprecipitation experiments.

This project will illuminate the extent to which Bunyaviruses hijack and manipulate protein trafficking within cells, enhancing our knowledge of how these viruses cause infection, as well as revealing novel cellular targets for therapeutic interventions against the severe human diseases caused by this family of viruses.

Dr Gemma Swinscoe - How do immunosuppressants affect innate immune responses in epithelial cells

For more details about the placement and how to apply, please read the job description

Transplant patients have an increased risk of acquiring viral infections such as the opportunistic pathogens BK polyomavirus and Cytomegalovirus which are often seen in renal transplants, or environmental exposure to seasonal or pandemic viruses. Infections in these patients results in prolonged recovery periods, and sometimes requires medical intervention which may be detrimental to the patient’s health. 

In patients taking immunosuppressants, the adaptive arm of their immune response is often severely weakened. This is the case in transplant patients, where it is desirable to suppress adaptive responses against the transplanted organ, requiring them to instead utilise their innate immune response. The innate immune response is robustly antiviral through the production of Interferons (IFNs).

However, it is currently unknown how immunosuppressants interact with this response. This is most under characterised in non-immune cells, such as epithelial cells which are the primary infection site of many viruses. It is important that we understand the interplay between immunosuppressants and epithelial cells, as it will improve characterisation of how immunosuppressed patients fight off infections and enable us to devise better clinical strategies to manage viral infections in these patients.

This project will aim to characterise the effects of commonly administered immunosuppressants; Tacrolimus (TAC) and Mycophenolate mofetil (MMF), on renal proximal tubule epithelial cells (RPTECs). This characterisation will be focus on three areas of interest:

Cell growth and survival. Treated RPTECs will be assayed for cell survival and proliferation, using cell viability and growth curve assays. This will be performed using a range of drug concentrations, which have been chosen based on therapeutic doses used in transplant patients.

Responsiveness to interferons and pathogens. Responsiveness of RPTECs under treatment will be investigated, using western blot and quantitative reverse transcriptase PCR (qPCR) analysis. Firstly, responsiveness to IFNs will be tested by endogenously adding recombinant IFNs to cells in culture, followed by testing responsiveness to pathogens, using immunostimulants which mimic viral DNA. In both cases qPCR will be performed for interferon stimulated genes, and western blot will be used to look at activation of IFN signalling cascades.

Permissiveness to infection with BK Polyomavirus (BKPyV). TAC and MMF treated RPTECs will be infected with BKPyV to observe the effect of immunosuppressants on virus replication. The effect on virus replication will be determined by immunofluorescence staining and western blotting for viral proteins.