Fixed-term

Understanding dysregulation of anti-bacterial lipopolysaccharide immunity in Type 1 diabetes

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Project Details: Bacterial lipopolysaccharide (LPS) and activation of Toll-like Receptor 4 (TLR4; aided by CD14 and MD-2) are important for reducing the risk of developing Type 1 diabetes in both mice and humans (1; 2). Part of this protection is believed to be through induction of an anti-inflammatory immune profile including IL-10. Furthermore, increases in the abundance of Bacteroidetes bacteria, which are dominant producers of LPS (3), can identify individuals at risk of, or living with, Type 1 diabetes, compared to individuals without Type 1 diabetes (4-10); however, LPS from these expanded Bacteroidetes bacteria are poor stimulators of TLR4 (3; 11). Additionally, our data indicate that LPS-sequestering proteins are altered in those with Type 1 diabetes, potentially further limiting the ability of LPS to activate TLR4 and induce anti-inflammatory IL-10 secretion by immune cells. The student selected for this PhD project will aim to understand: 1.    Whether LPS-sequestering proteins such as LBP, CD14 and anti-LPS antibodies reduce TLR4 signalling in immune cells in people with, or at risk of, Type 1 diabetes 2.    How structurally different LPS molecules from different bacterial donors influence anti-LPS immune responses 3.    Whether any of these anti-LPS immune markers could be novel biomarkers for identifying those at risk of developing Type 1 diabetes This project will involve working with a multidisciplinary team of researchers across Birmingham and Bristol in the UK and Indiana and Western Michigan in the USA to obtain key samples (serum/plasma and peripheral blood mononuclear cells) for study. The student will be trained in and learn many different experimental methods, including ELISA, flow cytometry, in vitro cell culturing and bioinformatic analyses. Work in vivo, in mice that develop spontaneous diabetes, may also be performed depending on the student’s interest. The student will join a growing World-leading Diabetes research team at the University of Birmingham comprising many PIs including Professor Parth Narendran, Professor Colin Dayan, Professor David Wraith, Dr Danijela Tatovic and Dr Pete Taylor among others. Person Specification Applicants should have a strong background in immunology, and ideally a background in type 1 diabetes/autoimmunity. They should have a commitment to research in studying the immune system and hold or realistically expect to obtain at least an Upper Second Class Honours Degree in a relevant subject. How to apply Informal enquiries and applications should be directed to Dr James Pearson – j.a.pearson@bham.ac.uk To apply, please send: •   A detailed CV, including your nationality and country of birth; •   Names and addresses of two referees; •  A covering letter highlighting your research experience/capabilities; •  Copies of your degree certificates with transcripts; •  Evidence of your proficiency in the English language, if applicable. Funding Notes This project is funded through the University of Birmingham 125th Anniversary Fellowship Scheme and a Breakthrough T1D grant. References 1. Vatanen T, Kostic AD, d’Hennezel E, Siljander H, Franzosa EA, Yassour M, Kolde R, Vlamakis H, Arthur TD, Hämäläinen AM, Peet A, Tillmann V, Uibo R, Mokurov S, Dorshakova N, Ilonen J, Virtanen SM, Szabo SJ, Porter JA, Lähdesmäki H, Huttenhower C, Gevers D, Cullen TW, Knip M, Xavier RJ, Group DS. Variation in Microbiome LPS Immunogenicity Contributes to Autoimmunity in Humans. Cell 2016;165:842-853 2. Gülden E, Ihira M, Ohashi A, Reinbeck AL, Freudenberg MA, Kolb H, Burkart V. Toll-like receptor 4 deficiency accelerates the development of insulin-deficient diabetes in non-obese diabetic mice. PLoS One 2013;8:e75385 3. d’Hennezel E, Abubucker S, Murphy LO, Cullen TW. Total Lipopolysaccharide from the Human Gut Microbiome Silences Toll-Like Receptor Signaling. mSystems 2017;2 4. Giongo A, Gano KA, Crabb DB, Mukherjee N, Novelo LL, Casella G, Drew JC, Ilonen J, Knip M, Hyöty H, Veijola R, Simell T, Simell O, Neu J, Wasserfall CH, Schatz D, Atkinson MA, Triplett EW. Toward defining the autoimmune microbiome for type 1 diabetes. ISME J 2011;5:82-91 5. de Goffau MC, Luopajärvi K, Knip M, Ilonen J, Ruohtula T, Härkönen T, Orivuori L, Hakala S, Welling GW, Harmsen HJ, Vaarala O. Fecal microbiota composition differs between children with β-cell autoimmunity and those without. Diabetes 2013;62:1238-1244 6. de Goffau MC, Fuentes S, van den Bogert B, Honkanen H, de Vos WM, Welling GW, Hyoty H, Harmsen HJ. Aberrant gut microbiota composition at the onset of type 1 diabetes in young children. Diabetologia 2014;57:1569-1577 7. Kostic AD, Gevers D, Siljander H, Vatanen T, Hyötyläinen T, Hämäläinen AM, Peet A, Tillmann V, Pöhö P, Mattila I, Lähdesmäki H, Franzosa EA, Vaarala O, de Goffau M, Harmsen H, Ilonen J, Virtanen SM, Clish CB, Orešič M, Huttenhower C, Knip M, Xavier RJ, Group DS. The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes. Cell Host Microbe 2015;17:260-273 8. Alkanani AK, Hara N, Gottlieb PA, Ir D, Robertson CE, Wagner BD, Frank DN, Zipris D. Alterations in Intestinal Microbiota Correlate With Susceptibility to Type 1 Diabetes. Diabetes 2015;64:3510-3520 9. Stewart CJ, Ajami NJ, O’Brien JL, Hutchinson DS, Smith DP, Wong MC, Ross MC, Lloyd RE, Doddapaneni H, Metcalf GA, Muzny D, Gibbs RA, Vatanen T, Huttenhower C, Xavier RJ, Rewers M, Hagopian W, Toppari J, Ziegler AG, She JX, Akolkar B, Lernmark A, Hyoty H, Vehik K, Krischer JP, Petrosino JF. Temporal development of the gut microbiome in early childhood from the TEDDY study. Nature 2018;562:583-588 10. Vatanen T, Franzosa EA, Schwager R, Tripathi S, Arthur TD, Vehik K, Lernmark Å, Hagopian WA, Rewers MJ, She JX, Toppari J, Ziegler AG, Akolkar B, Krischer JP, Stewart CJ, Ajami NJ, Petrosino JF, Gevers D, Lähdesmäki H, Vlamakis H, Huttenhower C, Xavier RJ. The human gut microbiome in early-onset type 1 diabetes from the TEDDY study. Nature 2018;562:589-594 11. Yoshida N, Yamashita T, Kishino S, Watanabe H, Sasaki K, Sasaki D, Tabata T, Sugiyama Y, Kitamura N, Saito Y, Emoto T, Hayashi T, Takahashi T, Shinohara M, Osawa R, Kondo A, Yamada T, Ogawa J, Hirata KI. A possible beneficial effect of Bacteroides on faecal lipopolysaccharide activity and cardiovascular diseases. Sci Rep 2020;10:13009

Modelling Ageing Blood Disorders Using Induced Pluripotent Stem Cells (iPSCs)

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Myelodysplastic syndromes (MDS) are a type of blood cancer that predominantly affect older adults, with a median age at diagnosis of 68 to 75 years. MDS originates at the level of haematopoietic stem/progenitor cells (HSPCs) and often progress to acute myeloid leukaemia (AML). There is no cure for MDS. Current therapies fail in 50-60% of patients, but how patients might be stratified to identify those likely to respond from those who fail therapy is not clear. Our group is interested on understanding the molecular mechanisms of disease progression and therapy resistance. Our work and the unique critical tools we have developed, including induced pluripotent stem cells (iPSCs) from patients with MDS, provide the opportunity to address these questions in the stem and progenitor compartment. This project will further investigate the contribution of specific mutations to the disease phenotype how these mutations influence genome instability in HSPCs and define the vulnerabilities this influence brings. Person Specification Applicants should have a strong background in stem cell/molecular biology. They should have a commitment to research in blood disorders and hold or realistically expect to obtain at least an Upper Second Class Honours Degree in a relevant subject. How to apply Applications should be directed to p.garcia@bham.ac.uk. To apply, please send: ·        A Detailed CV, including your nationality and country of birth; ·        Names and addresses of two referees; ·        A covering letter highlighting your research experience/capabilities; ·        Copies of your degree transcripts; ·        Evidence of your proficiency in the English language, if applicable. Applicants will be required to attend an interview. This can be conducted face –to –face, by telephone or skype Funding Notes This is for self-funded PhD students. In addition to the appropriate university fee (UK or international postgraduate research rate) the student will be expected to provide a bench fee of £20K approx., due to the high cost of iPSC cultures and differentiation to HSPCs. PhD projects will be of a total of 4 years, with 3.5 years in the lab and 6 months for thesis write-up. Any time in the write-up only mode will only incur a minimal tuition fee. References Lab website: https://www.birmingham.ac.uk/staff/profiles/cancer-genomic/garcia-paloma.aspx Apply Now

Research Fellow – School of Biosciences – 107238 – Grade 6

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Position Details School of Biosciences Location: University of Birmingham, Edgbaston, Birmingham UK Full time starting salary is normally in the range £33,002 to £35,608, with potential progression once in post to £39,906 Grade: 6 Full Time, Fixed Term contract up to September 2029 Closing date: 27 April 2026 This role is also open as an internal secondment opportunity which would need to be agreed by your current line manager. Background To assist in research (by carrying out data collection or analyses) to create knowledge through providing research support for projects and research groups. Role Summary A Research Assistant position is available in the research group of Prof. Carolina Rezaval at the University of Birmingham, UK. The successful candidate will contribute to research investigating how the brain prioritises behaviour when animals face conflicting internal needs and changing environmental demands. This position forms part of the Wellcome Trust Discovery Award programme “Decoding Competition in the Brain”, which builds on recent advances revealing how neuromodulatory circuits reshape decision-making under conflict (Cazalé-Debat, Scheunemann et al., Nature 2024; Day & Rezaval, Curr. Opin. Neurobiol. 2026). Using Drosophila melanogaster, we combine behavioural assays, neural circuit mapping, advanced genetics, two-photon imaging, and molecular approaches to uncover fundamental principles of behavioural choice. The postholder will work closely with members of the Rezaval lab. They will support experimental work including behaviour, microscopy, molecular biology, and Drosophila genetics, as well as routine fly work and laboratory organisation. The role will also involve analysing data and contributing to publications. The position offers broad training in neurogenetics and behaviour and is well suited to candidates wishing to develop towards a PhD. The post is available for an initial period of three years, with the possibility of extension. Main Duties •            Collect research data; this may be through a variety of research methods, such as scientific experimentation, literature reviews, and research interviews, under the supervision of Prof. Rezaval. •            Analyse research data as directed •            Present research outputs, including drafting academic publications or parts thereof, for example at seminars and as posters •            Develop or adapt techniques, models and methods •            Provide guidance as required to support staff and any students who may be assisting with research •            Deal with problems that may affect the achievement of research objectives and deadlines •            Carry out administrative tasks related directly to the delivery of the research •            Promotes equality and values diversity acting as a role model and fostering an inclusive working culture Person Specification •            First degree or equivalent professional qualification in an appropriate science subject (e.g. Life Sciences/Biological Sciences/Genetics/Cell Biology/Neuroscience/ Biochemistry or related disciplines). •            Practical experience of applying the relevant skills and techniques •            Ability to analyse information and communicate effectively •            Ability to access and organise resources successfully •            Knowledge of the protected characteristics of the Equality Act 2010, and how to actively ensure in day to day activity in own area that those with protected characteristics are treated equally and fairly Informal enquiries to Carolina Rezaval, email: c.rezaval@bham.ac.uk View our staff values and behaviours here Use of AI in applications: We want to understand your genuine interest in the role and for the written elements of your application to accurately reflect your own communication style. Applications that rely too heavily on AI tools can appear generic and lack the detail we need to assess your skills and experience. Such applications will unlikely be progressed to interview. Apply Now

Role of skeletal muscle stem cells in muscle aging

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Details The ability of skeletal muscles to regenerate in response to injury, exercise, growth or disease depends on a population of adult skeletal muscle stem cells called satellite cells. With aging, the number and regenerative capacity of the stem cells declines; this contributes to the aging process and ultimately to the loss of muscle mass in elderly people. Cell signalling plays a key role in controlling the balance between proliferation, differentiation and self-renewal (ability to maintain a stem cell pool) in skeletal muscle stem cells. Defects that disrupt this balance contribute to disease progression in muscular dystrophies and to aging. In previous work, we have uncovered a critical role for the Sonic Hedgehog signalling pathway in controlling the activity of skeletal muscle stem cells. However, the importance of this cell signalling pathway in aging remains to be established. Likewise, the cellular process(es) implicated in stem cell aging remain to be elucidated. This project consists in uncovering the mechanisms by which Sonic Hedgehog signalling controls skeletal muscle stem cells during muscle regeneration, and how disruption in Sonic Hedgehog signalling impacts muscle aging. The project will provide advanced training in stem cell biology (culture), molecular techniques (qPCR, RNAseq), imaging (confocal microscopy), and genetics (conditional knockout mouse lines). Science Graduate School As a PhD student in one of the science departments at the University of Sheffield, you’ll be part of the Science Graduate School. You’ll get access to training opportunities designed to support your career development by helping you gain professional skills that are essential in all areas of science. You’ll be able to learn how to recognise good research and research behaviour, improve your communication abilities and experience the breadth of technologies that are used in academia, industry and many related careers. Visit http://www.sheffield.ac.uk/sgs to learn more. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes Note that this project is for self-funded students only. Applicants should enquire about registration fees before applying. First class or upper second 2(i) in a relevant subject. To formally apply for a PhD, you must complete the University’s application form using the following link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying All applicants should ensure that both references are uploaded onto their application as a decision will be unable to be made without this information. References Cruz-Migoni SB, Mohd Imran K, Wahid A, Rahman O, Briscoe J, Borycki AG. A switch in cilia-mediated Hedgehog signaling controls muscle stem cell quiescence and cell cycle progression. BioRxiv doi: https://doi.org/10.1101/2019.12.21.884601 Jaafar Marican NH, Cruz-Migoni SB, Borycki AG (2016). Asymmetric Distribution of Primary Cilia Allocates Satellite Cells for Self-Renewal. Stem Cell Reports. 6(6):798-805. Apply Now

GPCR regulation of secretion in neuroendocrine cells

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Details G protein coupled receptors (GPCRs) remain one of the key therapeutic targets for the treatment of disease, and while much is known about their pharmacology, it is increasingly clear that the signaling mechanisms used by a specific receptor to modulate cell functions is context specific. Adrenal chromaffin cells have a vital role in the body’s response to stress; through the secretion of catecholamines they mediate the ‘fight-or-flight’ response resulting in increased heart rate, blood pressure and metabolic rate. This project aims to elucidate the molecular mechanisms used by GPCRs to modulate catecholamine secretion from chromaffin cells. Using a combination of patch clamp electrophysiology and live cell fluorescent imaging the interactions between heterotrimeric G protein subunits, their effectors and the protein machinery regulating vesicle docking, priming and fusion will be investigated. References https://www.sheffield.ac.uk/biosciences/people/academic-staff/elizabeth-seward Apply Now

Molecular Mechanisms used by GLP-1 Receptors to regulate secretion

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Details GLP-1 Receptor are G protein coupled receptors that naturally respond to glucagon-like peptide-1 (GLP-1), a hormone produced in the gut in response to food intake. The receptor is the target for the type 2 diabetes and weight loss drug semaglutide. Its actions in the pancreas are well studied however, little is known about the molecular mechanisms responsible for its regulation of secretion from neurons. Using a combination of high resolution live cell fluorescent imaging, electrochemistry and patch clamp electrophysiology, we recently discovered that activation of GLP-1Rs promotes the formation of stable fusion pores in adrenal chromaffin cells to facilitate peptide secretion. The aim of this project is to identify the signaling events and molecules controlling exocytosis which are regulated by GLP-1 receptors in neuro-endocrine cells. Investigations into ligand and location bias within this context could aid the development of the next generation of GLP-1 agonists for the treatment of diverse neurological and cardiovascular disorders. References GONZÁLEZ-SANTANA, A., ESTÉVEZ-HERRERA, J., SEWARD, E. P., BORGES, R. & MACHADO, J. D. 2021. Glucagon-like peptide-1 receptor controls exocytosis in chromaffin cells by increasing full-fusion events. Cell Reports, 36, 109609. https://www.sciencedirect.com/science/article/pii/S2211124721010470?via%3Dihub Seward Lab https://www.sheffield.ac.uk/biosciences/people/academic-staff/elizabeth-seward Apply Now

PhD Studentship: Preclinical modelling and therapeutic targeting of glioblastoma infiltrative margin

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Supervisors: Prof Ruman Rahman, Dr Stuart Smith, Dr Phoebe McCrorie Project Overview: Glioblastoma (GBM) is an incurable malignant brain tumour with severely limited therapeutic interventions and short survival times. Major challenges in treating GBM include intra-tumour heterogeneity and invasion into the adjacent healthy brain. Such invasive tumour subpopulations reflect residual disease intractable to standard multimodal treatment, and which is responsible for GBM recurrence. We have revealed distinct gene expression profiles of the infiltrative margin of glioblastoma via bulk transcriptomics https://pubmed.ncbi.nlm.nih.gov/37434262/ predicated on biopsies obtained via 5-aminolevulinic (5-ALA)-guided neurosurgery. We now aim to resolve infiltrative margin biology at high resolution using single cell and spatial transcriptomic methods, to identify actionable therapy targets which could lead to informed delivery of personalised medicine approaches. The appointed will work with genome, computational and cancer biologists at the University of Nottingham to develop and characterise patient-derived explant models amenable for drug repurposing studies. The project also introduces a collaboration with Queen’s Mary University, London, whereby 5ALA-negative astrocytes from the glioblastoma infiltrative margin will be re-programmed to generate induced pluripotent stem cells as a patient-matched toxicity control. Research Environment: Applications are invited for a 4-year fully-funded PhD studentship to join the University of Nottingham Brain Tumour Research Centre of Excellence (Director – Prof Ruman Rahman). The Centre is underpinned by 5-year programmatic funding from the charity ‘Brain Tumour Research (BTR)’ and represents a multidisciplinary and cross-Faculty research partnership, also leveraging international collaborators at University of Freiburg, Mayo Clinic Arizona, and Erasmus University Rotterdam. The hub of the Centre will be based at the Biodiscovery Institute (BDI) School of Medicine. Eligibility: BSc in cellular/molecular biology/biochemistry or related subject; MSc/MRes is desirable. Priority will be given to candidates with prior experience working with in vitro cancer models and associated drug inhibition assays. Those interested in applying should send a 2-page CV and 1-page cover letter to ruman.rahman@nottingham.ac.uk. Deadline: May 1st, 2026 Anticipated start date: July 1st, 2026. Funding notes: This 4-year PhD studentship will include tuition fees for home students and an annual stipend equivalent to current UKRI rates (starting at £22,123).

Investigating the Role of FIS1 in Regulating Mitochondria-Lysosome Contact Sites under Hypoxia

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Details Mitochondria-lysosome contact sites (MLCSs) are dynamic inter-organelle interfaces crucial for cellular homeostasis, facilitating metabolic exchange, organelle quality control and adaptive stress responses. Under hypoxic conditions, when oxygen levels are low, cells undergo significant mitochondrial remodelling. This includes increased formation of MLCSs and the emergence of megamitochondria engulfing lysosomes (MMEL), a process implicated in mitochondrial self-digestion and hypoxia adaptation. However, the molecular regulators of MLCS dynamics during hypoxia are poorly understood. FIS1 (Fission 1 protein) is a mitochondrial outer membrane protein best known for its role in mitochondrial division and mitophagy regulation. Recent studies reveal that FIS1, together with Mid51, also orchestrates MLCS dynamics by recruiting Rab7-GAPs (e.g., TBC1D15) to mitochondria, thereby promoting Rab7 inactivation and lysosome untethering. Loss of FIS1 disrupts this process, leading to abnormal lysosomal anchoring and impaired organelle organization. Despite these insights, the specific role of FIS1 in regulating MLCSs under hypoxia and facilitating cellular adaptation remains unclear. This project hypothesises that FIS1 regulates MLCS dynamics during hypoxia to coordinate mitochondrial remodelling, lysosomal reorganisation and cell survival. Three aims will be pursued using live/Fixed-cell imaging and biochemical assays: (1) characterise MLCS dynamics and the role of FIS1 under hypoxia; (2) determine how FIS1 affects mitochondrial morphology, MMEL, and protein degradation; and (3) assess the impact of FIS1-dependent MLCS regulation on lysosomal trafficking, mitochondrial quality control and hypoxia-induced cell death. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying By uncovering how FIS1 modulates MLCSs during hypoxic stress, this study will advance our understanding of organelle crosstalk and cellular resilience. Findings may also identify novel therapeutic targets for diseased conditions involving mitochondrial dysfunction and hypoxia, such as neurodegeneration, ischaemia and cancer. For more information about the project, or to discuss a potential application, please contact Dr Chun Guo (c.guo@sheffield.ac.uk) Science Graduate School As a PhD student in one of the science departments at the University of Sheffield, you’ll be part of the Science Graduate School. You’ll get access to training opportunities designed to support your career development by helping you gain professional skills that are essential in all areas of science. You’ll be able to learn how to recognise good research and research behaviour, improve your communication abilities and experience the breadth of technologies that are used in academia, industry and many related careers. Visit http://www.sheffield.ac.uk/sgs to learn more. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes First class or upper second 2(i) in a relevant subject. To formally apply for a PhD, you must complete the University’s application form using the following link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying All applicants should ensure that both references are uploaded onto their application as a decision will be unable to be made without this information. References https://www.sheffield.ac.uk/biosciences/people/academic-staff/chun-guo Hao, T. et al. Hypoxia-reprogramed megamitochondrion contacts and engulfs lysosome to mediate mitochondrial self-digestion. Nature Communications 14, 4105 (2023). https://doi.org:10.1038/s41467-023-39811-9 Waters, E. et al. The SUMO protease SENP3 regulates mitochondrial autophagy mediated by Fis1. EMBO reports 23, e48754 (2022). https://doi.org:https://doi.org/10.15252/embr.201948754 Wong, Y. C. et al. Mid51/Fis1 mitochondrial oligomerization complex drives lysosomal untethering and network dynamics. Journal of Cell Biology 221 (2022). https://doi.org:10.1083/jcb.202206140 Wong, Y. C., Ysselstein, D. & Krainc, D. Mitochondria–lysosome contacts regulate mitochondrial fission via RAB7 GTP hydrolysis. Nature 554, 382-386 (2018). https://doi.org:10.1038/nature25486 Zhao, A. et al. SENP3-FIS1 axis promotes mitophagy and cell survival under hypoxia. Cell Death & Disease 15, 881 (2024). https://doi.org:10.1038/s41419-024-07271-8 Apply Now

Molecular mechanism of plant organellar replication

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Details We invite applications for a PhD research project to study organellar protein-DNA interactions in plants. The projects will answer mechanistic questions about organellar genome duplication with downstream translational implications in developing better crops. Chloroplast is arguably the most important organelle for sustaining life as it is the main hub of photosynthesis, the process by which sunlight is converted to biomass. Chloroplast has its own genome, which codes for several key proteins involved in photosynthesis. Thus, accurate replication of the chloroplast genome is vital for photosynthesis and thus for life on earth. Yet, our understanding of chloroplast replication is in its infancy. In this collaborative, inter-disciplinary project we will combine cryo-EM and enzyme kinetics (Lahiri lab https://sites.google.com/sheffield.ac.uk/lahirilab/) with structural bioinformatics (Chaudhuri lab, https://www.sheffield.ac.uk/biosciences/people/academic-staff/roy-chaudhuri) and plant genetics (Casson lab, https://www.sheffield.ac.uk/biosciences/people/academic-staff/stuart-casson) to develop the first comprehensive picture of chloroplast replication. In addition to opening up a new dimension of understating of the fundamental process of organellar replication, insights gained from this work will aid downstream translational projects of chloroplast engineering to develop crops with better traits. Science Graduate School As a PhD student in one of the science departments at the University of Sheffield, you’ll be part of the Science Graduate School. You’ll get access to training opportunities designed to support your career development by helping you gain professional skills that are essential in all areas of science. You’ll be able to learn how to recognise good research and research behaviour, improve your communication abilities and experience the breadth of technologies that are used in academia, industry and many related careers. Visit http://www.sheffield.ac.uk/sgs to learn more. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes First class or upper second 2(i) in a relevant subject. To formally apply for a PhD, you must complete the University’s application form using the following link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying All applicants should ensure that both references are uploaded onto their application as a decision will be unable to be made without this information. References https://sites.google.com/sheffield.ac.uk/lahirilab/ https://www.sheffield.ac.uk/biosciences/people/academic-staff/roy-chaudhuri https://www.sheffield.ac.uk/biosciences/people/academic-staff/stuart-casson https://www.biorxiv.org/content/10.1101/2025.04.09.647933v1.full Apply Now

Illuminating the Plasmodium apicoplast genome organisation

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Details We invite applications for a PhD research project to study organellar protein-DNA interactions in human pathogens. The project will answer mechanistic questions about organellar genome organisation with downstream translational implications in combatting antimicrobial resistance. Plasmodium, the causative agent of malaria, harbours an essential non-photosynthetic plastid called the apicoplast. Just like mitochondria, apicoplast has its own genome and maintenance and compaction of the apicoplast DNA is essential for Plasmodium survival. Apicoplast genome is compacted by a prokaryotic histone like protein called HU. Sequence analysis reveals that the apicoplast HU has some major differences when compared to prokaryotic HU and our initial biochemistry shows that apicoplast HU uses unique mechanisms for apicoplast DNA compaction. In this collaborative, inter-disciplinary project, we will use cryo-EM (Lahiri lab https://sites.google.com/sheffield.ac.uk/lahirilab/), NMR (Willamson lab https://sites.google.com/sheffield.ac.uk/williamson/research?authuser=0) and single molecule biophysics (Newton lab https://www.sheffield.ac.uk/biosciences/people/academic-staff/matt-newton) to delineate the molecular mechanism of Plasmodium apicoplast genome organisation. In addition to answering a long-standing fundamental question, namely, how is organellar genome organised, the knowledge gained from this work will aid in downstream projects looking to develop inhibitors of apicoplast HU to combat multi-drug resistant Plasmodium. Science Graduate School As a PhD student in one of the science departments at the University of Sheffield, you’ll be part of the Science Graduate School. You’ll get access to training opportunities designed to support your career development by helping you gain professional skills that are essential in all areas of science. You’ll be able to learn how to recognise good research and research behaviour, improve your communication abilities and experience the breadth of technologies that are used in academia, industry and many related careers. Visit http://www.sheffield.ac.uk/sgs to learn more. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes First class or upper second 2(i) in a relevant subject. To formally apply for a PhD, you must complete the University’s application form using the following link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying All applicants should ensure that both references are uploaded onto their application as a decision will be unable to be made without this information. References https://sites.google.com/sheffield.ac.uk/lahirilab/ https://sites.google.com/sheffield.ac.uk/williamson/research?authuser=0 https://www.sheffield.ac.uk/biosciences/people/academic-staff/matt-newton https://www.biorxiv.org/content/10.1101/2025.04.09.647933v1.full Apply Now

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