Fixed-term

Job description Job Purpose To make a leading contribution to discovery and translational research exploring the role of creatine and homoarginine in cardiovascular health and disease. The post is laboratory based and funded by a British Heart Foundation programme grant awarded to Dr Craig Lygate. The post holder will have a PhD in a relevant discipline with extensive hands-on experience of standard biochemistry and molecular biology techniques, e.g. protein quantification, RT-PCR, molecular cloning and cell transfection. They will have the experience and depth of knowledge to develop new assays, troubleshoot when there are problems, and help supervise the work of others in the group. The post holder will contribute to the formulation and submission of research publications and proposals. Main Duties and Responsibilities Perform the following activities in conjunction with and under the guidance of the Principal Investigator: 1.      Plan and conduct research as outlined in the BHF programme grant and according to group and School research strategy. 2.      Document research outputs including analysis and interpretation of data, maintaining records and databases, drafting technical reports and papers as appropriate. 3.      Develop and enhance your research profile and reputation and that of the School and University, including establishing and sustaining a history of independent and joint publications in high quality international peer-reviewed journals. 4.      Presentation of work at international and national conferences, at internal and external seminars, webinars, colloquia, and workshops. 5.      Keep up to date with current knowledge and recent advances in the field (i.e. cardiac energetics, homoarginine metabolism, and myocardial biology). 6.      Take a leading role in the identification of potential funding sources and assist in the development of proposals to secure funding from internal and external bodies to support future research. 7.      Take a leading role in developing and maintaining collaborations with colleagues across the University and academic community. 8.      Take a leading role in team meetings and School research group activities to enhance the wider knowledge, outputs, and culture of the school. 9.      Take a leading role in the organisation, supervision, mentoring and training of undergraduate and postgraduate students and less experienced members of the project team to ensure their effective development. 10.  Perform administrative tasks related to the activities of the research group and School, including grant budgeting and writing/reviewing SOPs, risk assessments and Health & Safety documentation. 11.  Engage in personal, professional and career development, to enhance both specialist and transferable skills in accordance with desired career trajectory. 12.  Undertake any other reasonable duties as required by the Principal Investigator or Head of School. 13.  Contribute to the enhancement of the University’s international profile in line with the University’s Strategic Plan. Knowledge, Qualifications, Skills and Experience Knowledge/Qualifications Essential: A1.  Normally Scottish Credit and Qualification Framework level 12 (PhD) in biochemistry, biomedical sciences, pharmacology or equivalent plus track record of emerging independence within a research/professional environment, or alternatively possess professional qualifications and experience equivalent to PhD level plus the requisite experience A2. Specialist theoretical and practical knowledge of the following: protein biochemistry, cellular and molecular biology Desirable: B1. An up-to-date knowledge of the wider subject area of cardiovascular science B2. A UK Home Office Personal Licence (or equivalent training) Skills Essential: C1. Extensive practical skills in biochemistry and molecular biology techniques (e.g. protein & gene expression analysis, mammalian cell culture, molecular cloning, and the generation of transfected cell lines) C2. Excellent communication skills (oral and written), including public presentations and ability to communicate complex data/concepts clearly and concisely C3. Research creativity with the ability to develop key research collaborations C4. Excellent interpersonal skills including team working and a collegiate approach C5. Excellent organisational and time management skills C6. High level data analysis, statistical, and interpretation skills C7. Excellent problem-solving skills including a flexible and pragmatic approach C8. Clear ability to self-motivate and use initiative, working effectively as an individual C9. Excellent attention to detail and ability to work methodically Desirable: D1. Practical skills in HPLC D2. Practical skills in the study of protein post-translational modifications D3. Analysis of metabolomic and proteomic datasets Experience Essential: E1. Relevant research experience commensurate with an early career researcher E2. A track record of presentation of research results at conferences E3. Experience of scientific writing with a track record of first-author publications in quality journals E4. Contribution to researcher development, for example through the supervision of master’s and PhD students. E5. Contribution to the local research community via activities such as journal club presentation, committee membership etc. Informal Enquiries should be directed to Dr Craig Lygate, Craig.Lygate@glasgow.ac.uk ​ Terms and Conditions Salary will be Grade 7, £41,064 –  £44,746 per annum. Please note due to the available funding for this project we will be able to appoint the successful candidate for only up to SP35  £44,746. This post is full time (35 hours per week) and has funding for up to 10 May 2031 The University of Glasgow has a responsibility to ensure that all employees are eligible to live and work in the UK.  If you require a Skilled Worker visa to work in the UK, you will be required to meet the eligibility requirements of the visa route to be assigned a Certificate of Sponsorship. Please note that this post may be eligible to be sponsored under the Skilled Worker visa route if tradeable points can be used under the Skilled Worker visa rules. For more information please visit: https://www.gov.uk/skilled-worker-visa. As a valued member of our team, you can expect: 1 A warm welcoming and engaging organisational culture, where your talents are developed and nurtured, and success is celebrated and shared. 2 An excellent employment package with generous terms and conditions including 41 days of leave for full time staff, pension – pensions handbook https://www.gla.ac.uk/myglasgow/payandpensions/pensions/, benefits and discount packages. 3 A flexible approach to working. 4 A commitment to support your health and wellbeing, including a free 6-month UofG Sport membership for all new staff joining the University  https://www.gla.ac.uk/myglasgow/staff/healthwellbeing/. We believe that we can only reach our full potential through the talents of all. Equality, diversity and inclusion

Every day, we make choices that involve balancing opportunities with risks—but what’s actually happening in our brains as we make these decisions remains largely unknown. A central mystery in neuroscience is how the brain evaluates conflicting options and prioritizes specific actions. Evidence suggests there are sex differences in decision-making and unique vulnerabilities to neurological disorders across genders. Therefore, understanding how the brain makes decisions across contexts and genders holds important medical, economical, and societal benefits. Studying decision-making in mammals is challenging due to the brain’s complexity, but it is feasible in the fruit fly Drosophila, where single cells and circuits can be easily observed and manipulated. Capitalising on these advantages, we discovered a fascinating brain mechanism that allows flies prioritise behaviours during conflicting situations (Cazale-Debat et.al Nature, 2024 doi: 10.1038/s41586-024-07890-3). When animals, including humans, are deeply focused on something they desire—they may become less aware of potential dangers around them. This phenomenon, often referred to as “love blindness,” is a widespread behavioural tendency where the pursuit of a valued reward, like a mate, can overshadow possible risks. In the animal world, this kind of focus can help increase the chances of finding a mate and reproducing, but it also makes individuals more vulnerable to threats, such as predators. In our study, we explored how the brain balances risk and reward during courtship, focusing on male fruit flies. We discovered a neural mechanism controlled by dopamine, a chemical linked to reward and pleasure, which allows the flies to reduce their sensitivity to danger as they get closer to mating. In the early stages of courtship, visual signals alert the flies to nearby threats, activating certain neurons that cause the flies to stop courting. This response is mediated by serotonin, another brain chemical that temporarily inhibits the courtship drive to ensure survival. However, as the male flies advance in the courtship process, the brain gradually shifts gears. Dopamine levels rise, which reduces the response to threats, allowing the flies to stay focused on courtship instead of fleeing from danger. By tracking brain activity, we observed that the closer the flies get to mating, the higher the dopamine levels rise, eventually blocking the pathway that would normally alert them to visual threats. This allows the flies to “tune out” distractions and prioritise mating. In essence, dopamine acts as a sensory filter, adjusting the flies’ perception of threats based on their proximity to achieving their goal. This filtering system enables the brain to prioritise between competing actions, choosing reproduction over survival when it matters most. This PhD project will take this discovery further, aiming to answer key questions: (i) Does this dopamine-driven filtering mechanism also exist in females, and are there sex-specific differences? (ii) Is this neural mechanism applicable to other high-stakes decisions beyond mating versus predator avoidance? (iii) Is this neural mechanism an evolutionarily conserved strategy? As a PhD student on this project, you’ll work at the cutting edge of neuroscience, using state-of-the-art techniques including advanced genetics, neural circuit tracing/connectomics, multiphoton imaging to capture neural activity in live, synaptic tracing, behaving flies, optogenetics, CRISPR for gene editing, and custom coding for data analysis. You will collaborate with researchers working in Germany, UK and Switzerland. This project offers an unprecedented opportunity to uncover decision-making processes during conflicts at remarkable molecular, cellular, and neural circuit level, revealing fundamental principles of brain function across species and sexes. For more information about the Rezaval lab and research please visit: https://www.rezavallab.org/ Please contact Prof Rezaval directly with a cover letter outlining your interest, your background, and why you wish to join her lab in particular. References Mating proximity blinds threat perception. Nature (2024). https://doi.org/10.1038/s41586-024-07890-3. Laurie Cazalé-Debat*, Lisa Scheunemann*, Megan Day, Tania Fernandez-d.V. Alquicira, Anna Dimtsi, Youchong Zhang, Lauren A Blackburn, Charles Ballardini, Katie Greenin-Whitehead, Eric Reynolds, Andrew C Lin$, David Owald, and Carolina Rezaval. A neuronal mechanism controlling the choice between feeding and sexual behaviors in Drosophila. Cheriyamkunnel SJ*, Rose S*, Jacob PF, Blackburn LA, Glasgow S, Moorse J, Winstanley M, Moynihan PJ, Waddell S, Rezaval C. Curr Biol. 2021 Neuroscience: How the brain prioritizes behaviors. Barajas-Azpeleta, R, Tastekin I and Ribeiro C. Curr Biol. 2021. Bellen, H., Tong, C. & Tsuda, H. 100 years of Drosophila research and its impact on vertebrate neuroscience: a history lesson for the future. Nat Rev Neurosci 11, 514–522 (2010). https://doi.org/10.1038/nrn2839 Apply Now

In multi-cellular organisms, coordinated cell death (e.g. apoptosis) and cell replacement is critical for tissue recovery in response to stress or damage. Although there is not much known about this process at the cellular and molecular level, recent studies including ours have discovered that apoptotic cells can actively induce compensatory proliferation of surrounding cells through a non-apoptotic function of caspases, a family of cysteine-proteases that normally execute apoptosis. This research aims to dissect the molecular anatomy of compensatory cell proliferation following activation of apoptosis. By taking advantages of Drosophila as a model organism, we have developed unique assays to systematically identify and characterize regulators of compensatory cell proliferation. Because apoptosis-induced compensatory cell proliferation has been observed in tissue regeneration and tumorigenesis in multiple organisms including mammals, identification of its underlying regulatory mechanisms in Drosophila will significantly impact our understanding of its physiological role in tissue repair as well as its pathological role in multiple human diseases including cancer. State-of-the-art technologies in Cell Biology, Molecular Biology, Advanced Microscopy Imaging and Drosophila Genetics are employed in this research. Please provide a brief summary of your research experience when making inquiries or registering interest via FindAPhD. Alternatively, you can email the project’s lead supervisor directly with a CV outlining your education and relevant practical experience. To find out more about studying for a PhD at the University of Birmingham, including full details of the research undertaken in each school, the funding opportunities for each subject, and guidance on making your application, you can now order your copy of the new Doctoral Research Prospectus, at: https://www.birmingham.ac.uk/study/postgraduate Please find additional funding text below. For further funding details, please see the ‘Funding’ section. The School of Biosciences offers a number of UK Research Council (e.g. BBSRC MIBTP, https://www.birmingham.ac.uk/research/activity/mibtp/index.aspx) PhD studentships each year. Fully funded research council studentships are available to both UK nationals and overseas students. The deadline for applications for research council studentships is typically in early January each year. Each year we also have a number of fully funded Darwin Trust Scholarships. These are provided by the Darwin Trust of Edinburgh and are for non-UK students wishing to undertake a PhD in the general area of Molecular Microbiology. The deadline for this scheme is also typically in early January each year. Funding Notes All applicants should indicate in their applications how they intend to fund their studies. We have a thriving community of international PhD students and encourage applications at any time from students able to find their own funding or who wish to apply for their own funding (e.g. Commonwealth Scholarship, Islamic Development Bank). The postgraduate funding database provides further information on funding opportunities available at: https://www.birmingham.ac.uk/postgraduate/courses/research/bio/biosciences.aspx Applications to our competitive funding are normally closed in early January each year. Applicants with their own funding are welcome to apply at any time but must go through the same selection process. Please contact the project’s lead supervisor for further information. References 1) Farrell L, Puig-Barbe A, Haque MI, Amcheslavsky A, Yu M, Bergmann A and Fan Y. (2022) Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation. PLoS Genetics 18(12): e1010533. 2) Fan Y.*, Wang S., Hernandez J., Yenigun V.B., Hertlein G., Fogarty C.E., Lindblad J.L. and Bergmann A.* (2014) A model for identification of genes involved in apoptosis-induced proliferation in Drosophila. PLoS Genetics 10(1): e1004131. (*corresponding authors) 3) Fan, Y., and Bergmann, A. (2008) Distinct mechanisms of apoptosis-induced compensatory proliferation in proliferating and differentiating tissues in the Drosophila eye. Dev Cell 14, 399-410. Apply Now

About the Project Cancer and Wnt signaling: Cancer is a devastating disease affecting more than one in three people in the UK during their lifetime. Over 90% of colorectal cancers involve inappropriate activation of Wnt signaling, a fundamental pathway that controls when cells divide, differentiate, or die. Understanding how Wnt signaling is regulated is crucial for developing better cancer treatments with fewer side effects than current therapies. The scientific challenge: When Wnt molecules bind to their receptors (Frizzled and LRP5/6) on the cell surface, they cluster into structures called “signalosomes” that activate the pathway. Recent discoveries reveal these signalosomes are remarkably small and transient yet somehow generate sustained cellular responses lasting hours. This paradox—how brief receptor interactions produce prolonged signaling—represents one of the most significant unresolved questions in the field. Different studies have proposed conflicting mechanisms involving direct inhibition or various endocytic pathways, but the true mechanism remains unknown. Our research focus: We have identified potential links between actin cytoskeletal regulators and Wnt receptor signaling. Our data suggest these proteins may play a previously unrecognized role in regulating Wnt signaling through effects on receptor trafficking and localization. We hypothesize that cytoskeletal proteins facilitate receptor endocytosis and enabling sustained pathway activation beyond initial plasma membrane signaling events. What you will do: In this interdisciplinary project starting in June or October 2026, you will: ·       Investigate receptor endocytosis: Use CRISPR-Cas9 genome editing and advanced live-cell imaging techniques to study how Wnt receptors are internalized at physiologically relevant concentrations. You will determine which endocytic pathways are involved and evaluate the role of actin cytoskeletal regulators in this process. ·       Map spatial signaling: Employ fluorescent biosensors and super-resolution microscopy to determine where in the cell Wnt signaling is activated and sustained. You will use biochemical approaches to analyze signaling from different cellular compartments. ·       Quantify signaling outputs: Use reporter assays and protein analysis to measure how cytoskeletal-receptor interactions affect Wnt pathway activation. You will test the functional significance of these interactions using knockout and rescue approaches. ·       Validate in developing embryos: Perform experiments in Xenopus embryos using live imaging and functional assays to assess the physiological importance of these regulatory mechanisms during development. Impact and outcomes: Your work will identify actin cytoskeletal proteins as potential therapeutic targets for Wnt-driven cancers affecting millions globally. Unlike essential Wnt pathway components, these modulators may offer therapeutic windows for cancer-specific intervention with reduced side effects. Beyond cancer, this research will impact regenerative medicine by revealing how cytoskeletal control regulates tissue repair and stem cell maintenance. Research environment: You will join two friendly, collaborative labs embedded in the Randall Centre for Cell and Molecular Biophysics and the Centre for Craniofacial Development at King’s College London. We are part of the UK Cell Motility Club, which I am organising. The KCL Nikon Imaging Centre provides state-of-the-art microscopy facilities, and we collaborate with the European Xenopus Resource Centre in Portsmouth for developmental studies. Funding Notes Funding for entry in June or October 2026: Only self-funded students are eligible. Candidates must possess or be expected to achieve a 1st or upper 2nd class degree in a relevant subject of the biosciences. All applicants should indicate how they intend to fund their studies. We prefer candidates who have secured or wish to secure competitive funding from overseas government agencies. If you are interested in this project, please e-mail me (Matthias.Krause at KCL.AC.UK) with your CV and transcripts indicating how you plan to fund your studies. References Selected relevant publications:1. Cope, J.F.W., Law, A.-L., Juma, S., Sharpe, H.J., and Krause M. (2025) Nance-Horan Syndrome-like 1 interacts with endophilin and Ena/VASP proteins to promote fast endophilin-mediated endocytosis. BioRxiv, https://www.biorxiv.org/content/10.1101/2024.10.23.619882v32. Law, A.-L., Jalal, S., Pallett, T., et al., and Krause, M. (2021) Nance-Horan Syndrome-like 1 protein negatively regulates Scar/WAVE-Arp2/3 activity and inhibits lamellipodia stability and cell migration. Nature Communications, 12(1): 5687; DOI: 10.1038/s41467-021-25916-6.3. Dobson, L., Barrell, W.B., Seraj, Z., et al., Krause, M., Liu, K.J., (2023) GSK3 and Lamellipodin balance lamellipodial protrusions and focal adhesion maturation in mouse neural crest migration. Cell Reports, 42(9) DOI: 10.1016/j.celrep.2023.113030. *Co-senior authors4. Vehlow, A., Soong, D., Vizcay-Barrena, G., et al., and Krause, M. (2013) Endophilin, Lamellipodin, and Mena Cooperate to Regulate F-actin-dependent Endocytosis of the EGF-receptor. EMBO J. 32, 2722-2734.5. Krause, M. and Gautreau, A. (2014) Steering cell migration: lamellipodium dynamics and the regulation of directional persistence. Nature Reviews Molecular Cell Biology, 15, 577-90.

About the Project Cancer is a devastating disease: more than one in three people in the UK will develop cancer in their lifetime. Metastasis is the primary cause of cancer related deaths. Metastasis is caused by aberrant cell migration of cancer cells. We have identified NHSL1 as a key regulator of cell migration (Law et al., Nature Communications, 2021)9. NHSL1 is part of the poorly characterized Nance-Horan syndrome protein family. We showed that NHSL1 negatively regulates cell migration via the Scar/WAVE-Arp2/3 complexes which control actin filament nucleation required for cell migration9. Mechanistically, NHSL1 inhibits Scar/WAVE-Arp2/3 activity and consequently lamellipodia stability and cell migration efficiency9. In addition, we observed that NHSL1 localises to vesicles which emanate from the leading edge of migrating cancer cells suggesting that it is involved in vesicle trafficking9. Indeed, recently we showed that NHSL1 interacts with Ena/VASP proteins, key actin cytoskeleton regulators, and promotes fast endophilin-mediated endocytosis1,2. NHSL1 interacts with additional actin effectors (unpublished). During guided migration, growth factor receptors are endocytosed at the leading edge and traffic back there to increase polarity and directional migration. However, the molecular details of the pathways controlling this are still enigmatic. In this project, which will start in June or October 2026, you will investigate the role of NHSL1 in growth factor receptor recycling supporting directional migration of cancer cells. You will evaluate how NHSL1 interacts with additional actin effectors. You will use biochemistry to map and Gibson assembly to mutate the binding sites of these additional actin effectors. You will generate CRISPR-knockout cell lines and rescue them and existing NHSL1 CRISPR KO cell lines with cDNA mutated in the binding sites. You will utilise advanced imaging to track and quantify changes in the trafficking of the receptors. You will evaluate the functional significance of these interaction for chemotaxis of cancer cells using a well-established microfluidic chamber and using 3D invasion assays. Taken together, your PhD work will unravel a novel control mechanism of receptor recycling supporting cancer cell migration. You will join a friendly, interactive lab, which is part of the Cellular Biophysics Section of the Randall Centre at King’s College London: 11 laboratories with shared interest in the regulation of the cytoskeleton in cell division, adhesion, migration, and intracellular trafficking with joint meetings. Furthermore, our lab is part of the UK Cell Motility Club. Funding Notes Funding for entry in June or October 2026: Only self-funded students are eligible:  Candidates must possess or be expected to achieve a 1st or upper 2nd class degree in a relevant subject of the biosciences.  All applicants should indicate in their applications how they intend to fund their studies. We prefer candidates that have secured or wish to secure their own competitive funding from overseas government agencies.    If you are interested in this PhD project, please e-mail me (Matthias.Krause (at) KCL.AC.UK) with your CV and transcripts and indicate how you plan to fund your studies.   References Selected relevant publications: 1. Cope, J.F.W., Law, A.-L., Juma, S., Sharpe, H.J., and Krause M. (2025) Nance-Horan Syndrome-like 1 interacts with endophilin and Ena/VASP proteins to promote fast endophilin-mediated endocytosis. BioRxiv, https://www.biorxiv.org/content/10.1101/2024.10.23.619882v32. Narayan, K.B., James, H.P., Cope, J., Mondal, S., Baeyens, L., Milano, F., Zheng, J., Krause, M., and Baumgart, T. (2025) VASP phase separation with priming proteins of fast endophilin mediated endocytosis modulates actin polymerization. Journal of Biological Chemistry, DOI: 10.1016/j.jbc.2025.1108343. Casamento, A., and Boucrot, E., (2020) Molecular mechanism of Fast Endophilin-Mediated Endocytosis. Biochemical Journal, 477, 2327-2345.4. Wah Hak, L.C., Khan, S., Di Meglio, I., Law, A.-L., Häsler, S.L.A., Quintaneiro, L., Ferreira, A., Krause, M., McMahon, H., and Boucrot, E. (2018). FBP17 and CIP4 recruit SHIP2 and Lamellipodin to prime the plasma membrane for Fast Endophilin-Mediated Endocytosis. Nature Cell Biology, 20, 1023-1031.5. Carmona G, Perera U, Gillett C, Naba A, Law AL, Sharma VP, Wang J, Wyckoff J, Balsamo M, Mosis F, De Piano M, Monypenny J, Woodman N, McConnell RE, Mouneimne G, Van Hemelrijck M, Cao Y, Condeelis J, Hynes RO, Gertler FB, Krause M. (2016) Lamellipodin promotes invasive 3D cancer cell migration via regulated interactions with Ena/VASP and SCAR/WAVE. Oncogene. 2016 Sep 29;35(39):5155-69.6. Boucrot, E., Ferreira, A.P.A., Almeida-Souza, L., Debard, S., Vallis, Y., Howard, G., Bertot, L., Sauvonnet, N., and McMahon, H.T. (2015) Endophilin marks and controls a clathrin-independent endocytic pathway. Nature, 517, 7535, 460-465.7. Krause, M. and Gautreau, A. (2014) Steering cell migration: lamellipodium dynamics and the regulation of directional persistence. Nature Reviews Molecular Cell Biology, 15, 577-90 (2014).8. Vehlow, A., Soong, D., Vizcay-Barrena, G., Bodo, C., Law, A., Perera, U., and Krause, M. (2013) Endophilin, Lamellipodin, and Mena Cooperate to Regulate F-actin-dependent Endocytosis of the EGF-receptor. EMBO J. 32, 2722-2734.9. Law, A.-L., Jalal, S., Pallett, T., Mosis, M., Guni, A., Brayford, S., Yolland, L., Marcotti, S., Levitt. J.A., Poland, S.P., Rowe-Sampson, M., Jandke, A., Köchl, R., Pula, G., Ameer-Beg, S.M., Stramer, B.M., and Krause, M. (2021) Nance-Horan Syndrome-like 1 protein negatively regulates Scar/WAVE-Arp2/3 activity and inhibits lamellipodia stability and cell migration. Nature Communications, 12(1): 5687.10. Dobson, L., Barrell, W.B., Seraj, Z., Lynham, S., Wu, S., Krause, M.*, Liu, K.J.*, (2023) GSK3 and Lamellipodin balance lamellipodial protrusions and focal adhesion maturation in mouse neural crest migration. Cell Reports, 42(9). *Co-senior authors