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Research group

BiOmics

Bar coded DNA sample

Technological advances have allowed scientists to gather large amounts of data about a vast array of species, organisms and single cells. Our researchers are using mathematical modelling, machine learning and other algorithms to extract information and patterns from large data sets to further our understanding of disease.

Part of the Institute for Life Sciences

About

Contemporary scientific research benefits from rapid technological developments that enable the characterisation and quantification of biological molecules at unprecedented scale. Scientists can generate vast data that provide insight into the complex interplay of molecules within organisms. Interrogation and interpretation of these data inform the structure, function and interaction of molecules over time. 

We use ‘Omic technologies comprehensively to evaluate DNA (genomics), RNA (transcriptomics) and proteins (proteomics). We study small molecules using metabolomics. Microorganisms are investigated in a targeted manner using microbiomics or more broadly to characterise mixed samples using metagenomics.

At the University of Southampton, we generate vast datasets using these approaches across a wide range of environments and species. We work closely with NHS partners to use these capabilities to understand human disease and inform its clinical management. We bring together medical and biological scientists with mathematicians, computer and data scientists to develop and apply methods that exploit these data to their fullest potential.

From analysing patient genomes, to carrying out metagenomic analysis of water samples to using mass spectrometry metabolic profiling techniques, our scientists are studying the unique processes that take place within cells that can lead to disease or poor health outcomes in humans and help track changes in the environment.   

We are using data to answer clinical questions in areas such as cancer, autoimmune and respiratory diseases with the help of clinical colleagues we are translating our findings into novel techniques for clinicians to treat their patients, make predictions about prognosis and drug responsiveness.

Our researchers collaborate with partners at:

People, projects and publications

People

Dr Jay Amin BM, MRCPsych, PhD

Assoc Prof in Psychiatry of Older Age

Research interests

  • Developing our understanding of the role of inflammation in Lewy body dementia and Alzheimer's disease, including how it affects disease progression.
  • Undertaking cohort studies exploring clinical outcomes in dementia.
  • Undertaking clinical trials testing novel treatments in dementia.

Accepting applications from PhD students

Connect with Jay

Email: jay.amin@soton.ac.uk

Tel: +44 2380475206

ORCID

Dr Jeff Thompson

Lecturer

Research interests

  • Evolution of animal body plans
  • Macroevolution
  • Molecular Palaeobiology

Accepting applications from PhD students

Connect with Jeff

Email: J.R.Thompson@soton.ac.uk

ORCID

Dr Jennifer Williams

Lecturer

Research interests

  • Responsible and trustworthy audio processing applied to a variety of domains and use-cases;
  • Audio AI safety in terms of usability, privacy, and security;
  • Ethical issues of trust for audio AI (deepfake detection, voice-related rights, and speaker and content privacy). 

Accepting applications from PhD students

Connect with Jennifer

Email: J.Williams@soton.ac.uk

Tel: +44 7395826770

ORCID

Dr Jeremy Blaydes

Associate Professor

Research interests

  • Transcriptional responses to pathways: roles in the causes and treatment of cancer Intra-cellular stress-response pathways are activated in response to potentially deleterious conditions in the cell’s environment. In single celled organisms these pathways are generally involved in ensuring the survival and replication of the individual cell. In complex multi-cellular organisms such as man, they are critical in maintaining the normal function of each organ in the body, and the survival of the organism as a whole. Stress-response pathways play a key role in the patho-physiology and treatment of many diseases, including cancer.At almost every stage of the development of a tumour, cells are exposed to some form of stress. Examples include exposure to toxic compounds or radiation, loss of contact with other cells or the extra-cellular matrix, lack of oxygen (hypoxia), acidic pH, the activation of oncogenes, induction of cellular senescence, oxidative damage or depletion of essential metabolites. In some circumstances, the activation of a stress-response pathway will actually help the tumour cell to survive and proliferate. In other situations the response is cell cycle arrest or programmed cell death (apoptosis), providing a barrier to further tumour development that the tumour may ultimately circumvent through the acquisition of a mutation in one of the genes within the stress-response pathway. The p53 tumour suppressor protein is a key component of one such stress-response pathway, and virtually all cancers loose functionality of the p53-stress response pathway. Many current and prospective treatments for cancer work by either inhibiting, or re-activating stress response pathways.Our work focuses on the role of regulators of gene transcription in the response of cancer cells to stress. We have a long-standing interest in the p53 protein, a stress-activated transcriptional activator. We have also developed interests in other pathways which regulate gene transcription and cancer cell proliferation in response to stress and changes in cell metabolism. We aim to determine the role of these pathways in the development of cancer, and establish the potential for targeting components of the pathways for cancer therapy.Our group is based in the purpose-built Somers Cancer Research Building. Modern, well equipped laboratories provide us with an excellent research environment, and the opportunity to interact with researchers working on related areas of cancer biology.
  • Some Example Projects: Regulation of HDM2 and HDMX proteins The HDM2 oncoprotein is the major negative regulator of p53 function in the cell. In the late 1990s work from a number of groups, including Blaydes et al , demonstrated that HDM2 could be targeted in cancer cells to re-activate the p53 stress-response pathway. Subsequently, small molecule inhibitors of HDM2 have been developed that show great promise in pre-clinical trials. We have undertaken a series of projects examining how HDM2, and its paralogue HDMX is regulated in cancer cells (see Phillips et al, 2010, 2008, 2007, 2006a, 2006b and Phelps et al 2005, 2003). A particular interest of our work has been how HDM2 and HDMX protein synthesis is controlled in response to cell-signalling pathways in different cell types, and how this affects p53 function in these cells.
  • Role of CtBP transcriptional repressors in cancer cell proliferation and survival In common with p53, CtBP1 and CtBP2 proteins were discovered through their physical association with a viral oncoprotein. We have shown that CtBPs also interact with HDM2 protein, and can consequently regulate p53 function (Mirnezami et al, 2003). The main function of CtBPs is as transcriptional co-repressors. They are involved in a range of cellular processes, depending upon the transcriptional repressor that recruits them to DNA, and they suppress the transcription of genes that cause apoptosis (reviewed in Bergman et al, 2006a). CtBP activity is modified by UV radiation and glycolytic metabolism, suggesting that CtBPs regulate cell survival in response to cellular stress. From 2004 The Breast Cancer Campaign has funded work in our laboratory to study the role of CtBPs in breast cancer. Our studies have progressed from studies of the basic mechanisms whereby CtBPs control breast cancer proliferation and survival (Birts et al 2011 and Bergman et al 2009, 2006a) to their impact on the response to current chemotherapies (Birts et al 2010) to the demonstration that CtBPs are themselves a therapeutically tractable potential molecular target for cancer therapy (Birts et al 2013). Our group was named Breast Cancer Campaign “Team of the Year 2011” on the basis of this work.
Connect with Jeremy

Email: J.P.Blaydes@soton.ac.uk

Tel: +44 2381205170

ORCID

Professor Jeremy Frey

Professor of Physical Chemistry

Accepting applications from PhD students

Connect with Jeremy

Email: J.G.Frey@soton.ac.uk

Tel: +44 23 8059 3209

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ORCID
LinkedIn
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Professor Jeremy Webb

Professor of Microbiology

Research interests

  • Microbial biofilms and their control
  • Adaptive biology and evolution of microorganisms
  • Biofilm-associated infection

Accepting applications from PhD students

Connect with Jeremy

Email: J.S.Webb@soton.ac.uk

Tel: +44 23 8059 4390

ORCID

Miss Jessica Boxall

CORE eCRF Data Analyst

Research interests

  • Public Health
  • Nutrition
  • Food Security
Connect with Jessica

Email: J.L.Boxall@soton.ac.uk

ORCID
LinkedIn

Professor Jessica Teeling

Prof of Experimental Neuroimmunology

Research interests

  • Neuroimmunology
  • Systemic inflammation
  • Oral microbiome

Accepting applications from PhD students

Connect with Jessica

Email: J.Teeling@soton.ac.uk

Tel: +44 2381206103

ORCID

Professor Jim Anderson BA, PhD, PFHEA

Professor of Mathematics

Research interests

  • Hyperbolic space and its isometries
  • Kleinian groups (discrete groups of isometries of hyperbolic 3-space)
  • Signatures of actions of automorphism groups on Riemann surfaces

Accepting applications from PhD students

Connect with Jim

Email: J.W.Anderson@soton.ac.uk

Tel: +44 23 8059 5138

Google Scholar
ORCID
LinkedIn

Professor Jo Slater-Jefferies PhD, MBA, CMgr, MCMI

CEO-National Biofilms Innovation Centre
Connect with Jo

Email: josj@biofilms.ac.uk

Tel: +44 23 8059 4445

ORCID

Facilities

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We are at a very exciting time in Life Science Research. The potential for novel discovery using ‘omics technologies combined with the computer science methodologies is immense.
Professor Sarah Ennis
Professor of Genomics

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Contact us

Contact the Institute for Life Sciences team by emailing:
IfLSAdmin@soton.ac.uk