Fixed-term

Investigating how keratin networks modulate response to mechanical stress in healthy tissue and cancer

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Details Epithelial tissues are characterised by the expression of keratin proteins, which assemble into flexible, unbranched filaments to create complex cytoplasmic networks. These networks span across multiple cells, providing structural rigidity and allowing tissues to withstand mechanical forces. Keratins are less studied compared to other cytoskeletal filaments and their role in dictating the material properties of tissues and response to forces in proliferative tissues remains poorly understood. Abnormal keratin expression during cancer development can alter tissue mechanical properties and allow cancer cells to withstand compressive forces within a tumour environment. This PhD project aims to map keratin network architecture in epithelial monolayers and understand how they are reorganised in response to tissue stresses and during cancer development. Specifically, this project aims to: 1. Map keratin network architecture at super resolution in epithelial monolayers 2. Understand how keratin networks respond to local and tissue-scale forces 3. Understand how changes in keratin expression in cancer alter network organisation and response to force. This project will use state-of-the-art live-cell super resolution microscopy and automated image analysis to both visualise the 3D architecture of keratin networks in epithelial monolayers. You will explore how these networks influence tissue mechanical properties across scales and investigate their response to both local forces induced by cell divisions and tissue-scale stresses. You will then investigate how networks are altered following keratin switching in pancreatic cancer and whether this affects the ability of cells to withstand compressive forces using a mechanical confinement assay. This highly interdisciplinary project would suit a student with a background in either biophysics or biosciences, who is keen to develop skills in microscopy, quantitative image analysis and biophysical techniques. You will work together with a dynamic and friendly team of researchers across two different laboratories including cell biologists, biophysicists and computational experts. This project will give you the opportunity to develop cutting-edge imaging and analytical tools to answer fundamental biological questions about how tissues and tumours respond to mechanical stresses. Lab website: https://www.helenmatthewslab.org/ Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes Externally or self-funded students only Apply Now

Carbon Capture Crops

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Details To avoid climate breakdown, humanity urgently needs to design technologies to capture and store carbon. A widely proposed ‘nature-based’ solution is the enhancement of photosynthetic carbon-capture by plants but with a growing population, repurposing existing cropland for carbon sequestration is not feasible. A more likely scenario is the cultivation of novel crop cultivars that can both produce food and lock away stable carbon polymers. This project will study rice plants that have been genetically engineered to enhance CO2 uptake and fixation in the leaves and to produce stable carbon polymers in the roots. The study will be carried out in rice – a widely cultivated crop that is amenable to genetic manipulation. The results of this study will demonstrate the feasibility of generating new crop varieties that can enhance long-term storage of carbon in agricultural soils, without compromising on seed yield. However, genetically modified crops remain controversial, and the student will also explore emerging methods to produce similar ‘carbon-capture’ plants using gene-editing technology. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd/apply/applying Funding Notes Open to Self or externally funded students only. References https://sheffield.ac.uk/biosciences/people/academic-staff/julie-gray Apply Now

Population genomics of insect communities

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Details Declines in insect populations and species are arguably one of the most concerning symptoms of the biodiversity crisis, given their importance in underpinning food webs and ecosystem processes. Work in the Nadeau lab uses genomic tools to understand fundamental processes underpinning biodiversity, such as adaptation and speciation, primarily in tropical butterflies. We would be keen to recruit a PhD student, who has or is applying for external funding, and would be interested in working on projects using genomic data to understand levels of variation in insect populations in relation to environmental stressors such as temperature and pesticide use. There is scope for you to drive the direction of the project to suit your interests. Genetic variation underpins the ability of species of adapt to environmental challenges, and projects could address questions related to the genetic basis of adaption to environmental challenges. At the same time, environmental stressors can lead to a reduction in genetic diversity in populations, making them prone to inbreeding depression and limiting their ability to respond to further challenges. Therefore, projects could also address the impacts of environmental stressors on population genetic diversity. Projects could involve field work, experimental work, laboratory work and/or bioinformatic analysis of genomic data. You would receive training in the relevant techniques, as well as rigorous research and scholarly training throughout your PhD. You would be assigned a supervisory team who would provide research mentorship and pastoral support through your PhD journey. You would join a diverse and vibrant community of postgraduate students within the school of biosciences, with a wide range of opportunities for networking and career development. Funding Notes Self-funded project. Applicants would need to find their own funding. Apply Now

Identifying novel regulators of colorectal cancer invasion

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Details Cancer metastasis accounts for around 90% of cancer deaths. While the survival rate has been improved over the years through early diagnosis, limited progress has been made in the targeting of metastasis. This stems from a fundamental lack of understanding of the basic biology underlying this process. While flies have emerged as powerful tool to investigate tumour growth and identify cancer related pathways, to-date studies have been limited by a lack of metastatic models where cells can be followed from primary tumour development to secondary tumour formation in adult organisms. We recently overcame this longstanding limitation, developing the first model for the induction of macrometastases in adult Drosophila melanogaster. This project aims to now leverage this model to identify the cellular and molecular mechanisms that underlie the first steps of cell dissemination from the primary tumour. This will involve developing methods to live image tumour cell dissemination from primary tumours, and out of a complex organ, on our labs own dedicated multiphoton confocal. In parallel, genomics data existing within the lab will be mined to identify candidate genes. Combining live and fixed confocal analysis, as well as sensitive luciferase assays for each step of the metastatic process, these candidates will be investigated for a functional role in tumour metastasis. Overall, we expect the findings from the project to provide new insight into the complex process of cancer metastasis, as well as provide novel prognostic and therapeutic markers for metastatic colorectal cancer. Funding Notes Self-funding applicants only. References “Lab website https://cellplasticity.weebly.com/publications.html Recent publications from the lab Plygawko, A.T., Adams, J., Richards, Z. and Campbell, K. (2025) A hormonally regulated gating mechanism controls EMT timing to ensure progenitor specification occurs prior to epithelial breakdown. BioRxiv. doi: 10.1101/2025.07.19.665116 Montes-Labrador, M., Campbell, K. and Casali, A. (2025) Drosophila as a model for metastasis. Advances in Experimental Medicine and Biology. doi: 10.1007/978-3-031-97035-1_8. Jonckheere, S., Taminau, J., Adams, J., Haerinck, J., De Coninck, J., Verstappe, J., De Clercq, K., Peeters, E., Gheldof, A., De Smedt, E., Goossens, V., Audenaert, D., Candi, A., Versele, M., De Groote, D., Verschuere, H., Stemmler, M., Brabletz, T., Vandenabeele, P., Casali, A., Campbell, K., Goossens, S. and Berx, G. (2025). Development and validation of a high-throughput screening pipeline of compound libraries to target EMT. Cell Death and Differentiation. doi: 10.1038/s41418-025-01515-6. Plygawko, A.T, Stephan-Otto Attolini, C., Pitsidianaki, I., Cook, D.P., Darby, A.C and Campbell, K. (2024) The Drosophila adult midgut progenitor cells arise from asymmetric divisions of neuroblast-like cells. Developmental Cell. doi: 10.1016/j.devcel.2024.10.011 Parisi, E., Hidalgo, I., Montal, R., Pallisé, O., Tarragona, J., Sorolla, A., Novell, A., Campbell, K., Sorolla, M.A., Casali, A. and Salud, A. (2023) PLA2G12A as a novel biomarker for colorectal cancer with prognostic relevance. International Journal of Molecular Sciences. doi: 10.3390/ijms241310889. Sharpe, J.L., Morgan, J., Nisbet, N., Campbell, K. and Casali, A. (2023) Modelling cancer metastasis in Drosophila melanogaster. Cells. doi: 10.3390/cells12050677. Jonckheere, S., Adams, J., De Groote, D., Campbell, K., Berx, G. and Goossens, S. Epithelial-Mesenchymal Transition (EMT) as a therapeutic target. (2022) Cells Tissues Organs. doi: 10.1159/000512218 Pitidianaki, I., Morgan, J., Adams, J. and Campbell, K. (2021) Mesenchymal-to-epithelial transitions require tissue-specific interactions with distinct laminins. Journal of Cell Biology. doi: 10.1083/jcb.202010154 Adams, J., Casali, A. and Campbell K. (2021) Sensitive high-throughput assays for tumour burden reveal the response of a Drosophila melanogaster model of colorectal cancer to standard chemotherapies. International Journal of Molecular Sciences. doi: 10.3390/ijms22105101” Apply Now

From migration to morphogenesis: how cells stop moving and build epithelia

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Details Cells in development are constantly on the move — migrating to new locations, changing shape, and coordinating with their neighbours. But at some point, migratory cells must stop, polarise, and assemble into epithelial sheets to form organised tissues. How do cells decide when to make this transition from migration to building tissues, and how do their orientate and coordinate their behaviour with respect to their position in the embryo? This PhD project will focus on dissecting the external and internal factors driving a cell to stop moving become epithelial, guiding this fundamental switch during Drosophila midgut morphogenesis. You will use either existing single-cell transcriptomic atlases within in the lab, or carry out new single cell RNA-seq experiments to identify candidate pathways. You will then investigate for a functional role using deep-tissue live and fixed imaging on our lab’s own dedicated dual-line multiphoton confocal combined with cell and genetic approaches routinely performed in the lab, such as FISH and CRISPR. There will also be the chance to build on techniques we have recently started using in our system, such as expansion microscopy and laser ablation combined with live imaging. This is a unique opportunity for you to carry out cutting-edge microscopy and develop your skills in an exciting multidisciplinary environment. Funding Notes Self-Funded applicants only References “Lab website https://cellplasticity.weebly.com/ Recent work from the lab Plygawko, A.T., Adams, J., Richards, Z. and Campbell, K. (2025) A hormonally regulated gating mechanism controls EMT timing to ensure progenitor specification occurs prior to epithelial breakdown. BioRxiv. doi: 10.1101/2025.07.19.665116 Plygawko, A.T, Stephan-Otto Attolini, C., Pitsidianaki, I., Cook, D.P., Darby, A.C and Campbell, K. (2024) The Drosophila adult midgut progenitor cells arise from asymmetric divisions of neuroblast-like cells. Developmental Cell. doi: 10.1016/j.devcel.2024.10.011 Sharpe, J.L., Morgan, J., Nisbet, N., Campbell, K. and Casali, A. (2023) Modelling cancer metastasis in Drosophila melanogaster. Cells. doi: 10.3390/cells12050677. Jonckheere, S., Adams, J., De Groote, D., Campbell, K., Berx, G. and Goossens, S. Epithelial-Mesenchymal Transition (EMT) as a therapeutic target. (2022) Cells Tissues Organs. doi: 10.1159/000512218 Pitidianaki, I., Morgan, J., Adams, J. and Campbell, K. (2021) Mesenchymal-to-epithelial transitions require tissue-specific interactions with distinct laminins. Journal of Cell Biology. doi: 10.1083/jcb.202010154 Plygawko, A.T., Kan, S., and Campbell, K. (2020) Epithelial–mesenchymal plasticity: emerging parallels between tissue morphogenesis and cancer metastasis. Philosophical Transactions of the Royal Society B: Biological Sciences, Vol. 375, No. 1809. doi: 10.1098/rstb.2020.0087. Apply Now

Evolutionary genetics in a wild mammal population

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Details The project will use genomic and epigenetic datasets to address evolutionary questions in one of the best-studied wild mammal populations anyway in the world – the Soay Sheep population of St Kilda, Scotland. There is considerable flexibility to propose and develop a research question, with support from the supervisor. Most of our work combines genomic, epigenetic and life history data to try to tease apart the effects of genes and environment on phenotypic variation. We have recently developed an interest in epigenetic clocks as tools to understand ageing and the effects of environmental variation on traits related to fitness and survival. There will be the possibility of carrying out field work on St Kilda, as well as labwork opportunities. An interest in exploring, analysing and interpreting genomics datasets is a necessity, although training on that will be given. 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. 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 Jon Slate: https://www.sheffield.ac.uk/biosciences/people/academic-staff/jon-slate Soay Sheep Project: https://biology.ed.ac.uk/soaysheep Apply Now

Unravelling alternative cancer metabolic pathways

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Details The surface of cancer cells is a unique environment to study, as it is the gatekeeper for the uptake of nutrients and drugs. The turn-over and organisation of proteins at the plasma membrane is an essential part of cellular regulation. Many cell surface proteins have been implicated and play a role in disease progression. Using an siRNA targeted screen for novel drug uptake mechanisms, we have identified a class of receptors enriched on the surface of cancer cells that appear to also play a role in metabolic regulation. Little is known about some of these receptors or how and why their expression is unregulated. However, clinical reports suggest that higher expression in patients leads to a poor prognosis. Our group is highly invested in understanding their molecular and cellular biology. This project will investigate the expression, internalisation and signalling of these membrane proteins. We would like to investigate these as potential new cancer targets for drug discovery. This PhD will investigate the role of these receptors in cancer growth and progression using microscopy, cellular and molecular techniques. You will gain hands-on expertise in cutting-edge techniques, including: advanced cell microscopy at the Wolfson Light Microscopy Facuilty, using confocal and super-resolution (SIM and STORM) systems, alongside data analysis tools and expert scientific support. You will use quantitative cellular assays, and sophisticated molecular biology tools creating receptor mutants using CRISPR and knock-downs with siRNA. We’re seeking a highly motivated and curious scientist with a strong foundation in Pharmacology, Biochemistry, Cell Biology, or Molecular Biology. If you are passionate about translational science and want your research to have a tangible impact on the fundamental science underpinning human health please contact us. The School of Biosciences at the University of Sheffield hosts ~240 PhD students and you’ll be based in the Molecular and Cellular Biology Research Cluster. You’ll get access to professional training opportunities designed to support your career development, including communication and technology skills that are essential in academia, and industry. Visit http://www.sheffield.ac.uk/sgs to learn more. Funding Notes Please note this is for Self-Funded students only References Hadianamrei R, et al., (2023) Biochem Biophys Res Commun. doi: 10.1016/j.bbrc.2023.02.026 Cirillo S, et al., (2024) Eur J Pharm Biopharm. doi: 10.1016/j.ejpb.2024.114244 Brown Laboratory https://sheffield.ac.uk/biosciences/people/academic-staff/stephen-brown

Regulation of bacterial adherence to human cells by ZDHHC5-mediated S-acylation of cell surface proteins.

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Details This project will investigate the role of ZDHHC5, a cell surface-localised protein S-acyltransferase, in regulating cell adhesion and bacterial adherence to human cells. ZDHHC5 is one of 23 human DHHC enzymes responsible for attaching fatty acids to proteins, a process known as S-acylation (or palmitoylation). This modification is reversible and dynamically regulates protein trafficking, stability, and function. We hypothesise that ZDHHC5-mediated S-acylation of key adhesion proteins is a crucial regulatory mechanism for bacterial adherence to human cells. The project aims to identify and quantify the specific protein substrates of ZDHHC5 that are involved in cell-cell adhesion, as cell adhesion pathways are often commandeered for bacterial adherence to host cells. The project will also determine if these protein substrates are utilised in cell-bacterial adhesion and investigate how ZDHHC5-mediated S-acylation affects bacterial binding to human cells. This project will utilise a combination of molecular and cell biology approaches, microbiology and advanced quantitative proteomic methods. ZDHHC5 knockout cells will be used to study the perturbed cell surface proteome and how this leads to a bacterial adherence phenotype. Direct S-acylation substrates of ZHHC5 will be identified using a mass spectrometry-based proteomics method that we have developed. Specific proteins identified from this screen will be validated using siRNA-mediated knockdown and CRISPR knockout in bacterial adherence assays to determine which specific cell surface proteins mediate interactions with bacteria. Understanding the mechanism by which ZDHHC5 regulates interactions between cells and how it controls bacterial adherence and traversal will help to develop new strategies to combat infectious diseases, especially in the face of growing antibiotic resistance. It would enable the creation of novel therapeutic and preventative measures that target the initial, critical step of infection. Funding Notes Self-Funded students only, you will need to have your own funding. 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 Wolverson PA, Fernandes Parreira I, Thompson RH, Collins MO, Shaw JG, Green LR. Dynamics of the CD9 interactome during bacterial infection of epithelial cells by proximity labelling proteomics. FEBS J. 2025 Oct 17. doi: 10.1111/febs.70291. Woodley KT, Collins MO. S-acylated Golga7b stabilises DHHC5 at the plasma membrane to regulate cell adhesion. EMBO Rep. 2019 Oct 4;20(10):e47472. doi: 10.15252/embr.201847472 https://sheffield.ac.uk/biosciences/people/academic-staff/mark-collins Apply Now

Identifying climate-proof mechanisms of plant acclimation to freezing temperatures

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About the Project Climate change brings many challenges for the planet’s plants and one of these is the vulnerability caused by erratic temperatures. Many plants, including major crops, prepare for winter through a process called cold acclimation. In this process, plants respond to the cooler temperatures that prevail in the autumn, by making changes that equip them with resilience against subsequent freezing conditions in winter. This powerful mechanism is now under threat, as harsh frosts often occur without warning, after very warm days. This is particularly prevalent in the spring and is responsible for significant crop losses in temperate countries. This project follows on from our recent discovery that plants can use high levels of light to bring about increased freezing tolerance. The successful candidate will perform a wide range of genetic, metabolic and physiological analyses to identify the steps in cold acclimation that can be brought about by high light levels and will determine whether high light has this effect through increasing levels of photosynthesis or by upregulating the classical cold acclimation pathway. Genes encoding key proteins that are important to the high light-dependent pathway will be identified. The student will then engage in evolutionary analysis of these proteins. This will help us understand whether the ability to use high light as a cold acclimation signal, in the absence of cool autumn temperatures, varies across plant species depending on their habitat. The long-term goal of this research is to produce crop plants that are more resilient to spring frosts and are able to use information other than temperatures to trigger increased freezing tolerance. Understanding this mechanism could help farmers protect crops from climate change-related frost damage, improving food security. You will gain expertise in plant physiology, molecular biology, bioinformatics, and gene editing. Project structure: We have recently demonstrated that 5-day high-light treatment acclimates photosynthetic electron transport (PET, operating efficiency of PSII Fq’/Fm’) and enhances freezing tolerance in the absence of cold acclimation. Whether high light acclimation facilitates acclimation to freezing by activating recognised and/or novel cold-responsive signalling or by increasing energy production remains unknown. This project will investigate the basis for this phenomenon. Objective 1: Determine how PET acclimation under high light conditions augments freezing tolerance. (a) Using inhibitors for specific PET components and dark treatment to fully inhibit light reactions, the role of PET acclimation will be addressed. (b) PET measurements, infrared gas analysis (IRGA) for CO₂ assimilation, metabolite quantification, and marker gene expression will be compared during CA and HLA. This will identify mechanistic differences to reveal high light pathway-specific steps. (c) Testing Arabidopsis mutants of light signalling components for CA response will reveal CA dependency on light-responsive proteins. Objective 2: Identify ecotypic variation in high light acclimation response with increased freezing tolerance. Natural Arabidopsis ecotypes from diverse environments will be assessed by measuring parameters from 1a and measurement of freezing tolerance. This will reveal whether the ability to use HLA as a proxy for CA might vary with natural habitat. Genomes of accessions showing contrasting behaviours will be analysed for variation at candidate gene loci identified above. This part of the work will be undertaken with our collaborator Dr Maxim Kapralov, University of Newcastle, who will co-supervise the student. Objective 3: In vivo and in silico analysis of candidate genes. Candidate genes will be investigated using reverse genetics. The student will perform complementary evolutionary analysis of candidate gene homologues from diverse angiosperms in different climates (available in GenBank) within phylogenetic analyses frameworks for positive selection (with MK, Newcastle). This will pinpoint potential amino acid switches within proteins responsible for increased HL-mediated cold acclimation. SNPs encoding such switches will be queried empirically by complementing complete loss-of-function mutants with modified sequences and testing CRISPR-Cas modified plants for freezing tolerance. Funding Notes If you are interested in applying, in the first instance contact the supervisor Prof Heather Knight, p.h.knight@durham.ac.uk, with a CV and covering letter, detailing your reasons for applying for the project. References 1. Irabonosi Obomighie, Iain J. Prentice, Peter Lewin-Jones, Fabienne Bachtiger, Nathan Ramsay, Chieko Kishi-Itakura, Martin W. Goldberg, Tim J. Hawkins, James E. Sprittles, Heather Knight & Gabriele C. Sosso (2025) Understanding pectin cross-linking in plant cell walls. Communications Biology volume 8, Article number: 72 (2025). 2. Paige E Panter, Jacob Seifert, Maeve Dale, Ashley J Pridgeon, Rachel Hulme, Nathan Ramsay, Sonia Contera, Heather Knight (2023) Cell wall fucosylation in Arabidopsis influences control of leaf water loss and alters stomatal development and mechanical properties. Journal of Experimental Botany, Volume 74, Issue 8, 18 April 2023, Pages 2680–2691. 3. Robyn A Emmerson, Phillip Davey; Mouesanao Kandjoze, Ulrike Bechtold, Nicolae Radu Zabet, and Tracy Lawson (2025) DNA methylation contributes to plant acclimation to naturally fluctuating light, New Phytologist, accepted. 4. Alvarez-Fernandez, Ruben; Penfold, Christopher; Galvez-Valdivieso, Gregorio; Exposito-Rodriguez, Marino; Bowden, Laura; Moore, Jonathan; Mead, Andrew; Davey, Phillip; Matthews, Jack; Wild, D; Lawson, Tracy; Bechtold, Ulrike; Denby, Katherine; Mullineaux, Philip (2021) Time series transcriptomics reveals a BBX32-directed control of dynamic acclimation to high light in mature Arabidopsis leaves, The Plant Journal 107: 1363–1386. 5. Iqbal WA, Miller IG, Moore RL, Hope IJ, Cowan-Turner D, Kapralov MV. (2021) Rubisco substitutions predicted to enhance crop performance through carbon uptake modelling. J Exp. Bot 72:6066-6075

Development of chemical genetic tools to characterise the response to perturbation of protein folding homeostasis in the endoplasmic reticulum

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About the Project A self-funded PhD studentship to develop chemical genetic tools to study signal transduction in the unfolded protein response in human cells is available in the group of Dr. Martin Schröder in the Department of Biosciences at Durham University, Durham, United Kingdom. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) causes ER stress and activates a signalling network called the unfolded protein response (UPR) [1, 2]. ER stress and the UPR contribute to the onset and progression of many diseases including neurodegenerative diseases such as Alzheimer’s or Parkinson’s disease or metabolic diseases, for example diabetes. Three proximal ER stress sensors, ATF6, IRE1, and PERK initiate signalling events in the UPR [1, 2]. The bifunctional protein kinase-RNase IRE1 is a key signalling molecule in the UPR. The RNase domain of activated IRE1α initiates non-spliceosomal splicing of the mRNA for the transcription factor XBP1 [3]. The protein kinase domain of IRE1 controls the activity of its RNase domain. The successful candidate will develop a chemical genetic system that will allow activation of IRE1 without activation of either ATF6 or PERK or the accumulation of unfolded proteins in the ER. This chemical genetic system will allow investigation of signalling events downstream of IRE1 in isolation as well as investigation of how, and if at all, downstream signalling events initiated by IRE1 are modulated by activation of other ER stress sensors or unfolded proteins in the ER. To this end the student will use molecular genetic approaches to generate new stably transfected mammalian cell lines, reverse transcriptase PCR and quantitative PCR to study processing of XBP1 mRNA and other mRNA substrates by IRE1, immunoprecipitation/Western blotting techniques to characterise the phosphorylation status of IRE1, and fluorescence microscopy to characterise the subcellular distribution of IRE1 in unstressed cells and cells experiencing endoplasmic reticulum stress. The student will be trained in cloning, state-of-the-art molecular genetic and molecular biology techniques, as well as biochemical and cell biological techniques, including electrophoresis of proteins, Western blotting and immunoprecipitation techniques to characterise the phosphorylation status of IRE1α or cell-based assays to monitor cell viability and activation of cell death programs. Applicants should possess at least a 2:1 Honours degree, or equivalent, in an appropriate subject (e.g. biochemistry, cell biology, molecular biology, or genetics). Funding Notes If you are interested in applying, send your CV and covering letter detailing your reasons for applying for this studentship to the prospective project supervisor, Dr. Martin Schröder, at martin.schroeder@durham.ac.uk. References 1. Hetz, C., K. Zhang, and R.J. Kaufman, Mechanisms, regulation and functions of the unfolded protein response. Nat Rev Mol Cell Biol, 2020. 21(8): p. 421-438. 2. Read, A. and M. Schröder, The Unfolded Protein Response: An Overview. Biology (Basel), 2021. 10(5): p. 384. 3. Yoshida, H., et al., XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor. Cell, 2001. 107(7): p. 881-91

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