Fixed-term

We invite enthusiastic applicants for a 2½-year Postdoctoral research position in Environmental Toxicology with a focus on chemical imaging. The position is funded by the EU Partnership for Risk Assessment of Chemicals (PARC), Carlsberg Foundation, and SDU. The project will be carried out in the Ecotoxicology group at the Department of Biology, University of Southern Denmark (SDU). The starting date for the position is as soon as possible, no later than November 2026.  Project backgroundExposure to endocrine-disrupting chemicals (EDCs), including those released from micro- and nanoplastics such as substituted phenols (e.g., BPA and BPA alternatives) and PFAS, in the environment is invisible but inevitable. However, there are large gaps in our understanding of the mechanistic events that lead to adverse effects on individual animals and populations. EDCs affect both vertebrates and invertebrates, and the project will investigate their effects in biological samples from multiple species after exposure to known or suspected EDCs using advanced chemical imaging. Special focus will be on the effects of substituted phenols in vertebrates and on chemicals that disrupt molting in arthropods. The research builds on the Danish Sapere Aude TriOOL project and the Carlsberg Research Infrastructure project, which combines comparative embryo models, biochemical imaging, molecular analyses, and toxicological assessment to revolutionize our understanding of micro- and nanoplastics’ environmental and health impacts. A central research platform will be SDU’s photothermal chemical imaging system, which integrates optical photothermal infrared spectroscopy, simultaneous Raman spectroscopy, and co-located fluorescence imaging. This combination enables label-free chemical identification and high-resolution spatial mapping of plastics and associated chemicals in complex samples as well as mapping of exposure-associated changes in lipid organization, protein secondary structure, or cellular biochemical fingerprints within endocrine responsive tissues. The platform fosters a strong community that includes the Danish Center for Hadal Research, the Danish Center for Research in Marine Plastic Pollution, the Danish Molecular Biomedical Imaging Center, and the Natural History Museum of Denmark. The project is led by Associate Professor Dr. Elvis Genbo Xu and Associate Professor Dr. Henrik Holbech. The PARC project team includes top-level collaborators such as Prof. Knut Erik Tollefsen (Norway), Prof. Dries Knapen (Belgium), and Prof. Terje Svingen (Denmark).    QualificationsWe seek an enthusiastic, ambitious, and independent candidate with a PhD in spectroscopy, analytical chemistry, microscopy, environmental toxicology, biology, biophysics, materials science, or a related field, and demonstrated expertise in infrared or Raman spectroscopy, chemical imaging, spectral analysis, or image analysis. Experience with O-PTIR, FTIR imaging, Raman mapping, chemometrics, micro- and nanoplastics, biological samples, Python, R, or MATLAB is highly desirable. The candidate should possess strong experimental skills, scientific independence, and excellent English communication skills. ResponsibilitiesThe postdoctoral researcher will: Develop and validate O-PTIR, Raman, and fluorescence imaging methods. Analyze micro- and nanoplastics in biological and environmental samples. Process spectral and imaging data using chemometrics and multivariate statistics. Integrate imaging results with toxicological and molecular endpoints. Publish findings and collaborate within the PARC and SDU’s Photothermal Chemical Imaging platform networks. Additional information about the position is available from Dr. Elvis Genbo Xu, e-mail: elvis@biology.sdu.dk. Website: https://portal.findresearcher.sdu.dk/en/persons/elvis  SDU and the Ecotoxicology groupUniversity of Southern Denmark (SDU) was founded in 1966 as a top research and educational institution in Denmark, with strong contacts with international industries and the scientific community. It is both the third-largest and the third-oldest Danish university. Several international reports testify that SDU conducts world-class research and ranks it as one of the Top 50 young universities in the world. As a fast-growing young university, SDU now has five faculties and over 30,000 students, more than 15% of whom come from abroad. More than 1,200 researchers are divided into five faculties, 32 departments, and 11 research centers.  The position will be based in the Ecotoxicology group at the Department of Biology, SDU, in Odense. The Postdoctoral Researcher will have strong support from the Ecotoxicology group, which is well recognized for 30 years of research excellence in developing ecotoxicological approaches and assessing the risks of environmental contaminants, including heavy metals, endocrine-disrupting chemicals, pesticides, and pharmaceuticals, as well as from broad networks in the EU and beyond. We recommend that as an international applicant, you take the time to visit Work in Denmark where you will find information and facts about moving to, working and living in Denmark, as well as the International Staff Office at SDU. Application, salary etc.The successful applicant will be employed in accordance with the agreement between the Ministry of Finance and AC (the Danish Confederation of Professional Associations). Please check links for more information on salary (only available in Danish) and  taxation. Salary is determined in accordance with the applicable collective agreement and based on objective and gender-neutral criteria, including the content of the position, responsibilities, and qualification requirements.As an applicant, you are entitled to information about the starting salary and salary range for the position. This information will be provided during the recruitment process.SDU does not collect information on applicants’ previous salary. The application must include the following: A curriculum vitae including information on previous employment with start and end dates  A full list of publications stating the scientific publications on which the applicant wishes to rely Copy of PhD diploma, if Phd diploma has not yet been received, please include statement from your supervisor Shortlisting may be used in the assessment process. Incomplete applications and applications received after the deadline will neither be considered nor evaluated. To qualify you must have passed a PhD or equivalent. Applications will be assessed by an expert assessor/committee. Applicants will be informed of their assessment by the university. The University wishes our staff to reflect the diversity of society and thus welcomes applications from all qualified candidates regardless of personal background. Applications must be submitted electronically using the link “Apply now“. Attached files must be in Adobe PDF format. We strongly recommend that you read How to apply for a position at SDU before you apply.If you experience technical problems, please contact hcm-support@sdu.dk Further information for international applicants about entering and working in Denmark. About SDUThe University of Southern Denmark was established to create value for and with society. Whether our contributions come in the form of excellent research, innovative solutions, education or learning, we

 Dr M Higgs Application Deadline: Applications accepted all year round Details Our genomic DNA is under constant attack from DNA damaging agents, which are a continuing threat to genomic integrity. Defective resolution of DNA damage underlies several human diseases, including neurological abnormalities and developmental disorders as well as cancer. To counteract this, multiple DNA damage response (DDR) proteins act to combat DNA damage, by detecting DNA damage, activating cell cycle checkpoints, and promoting the repair/resolution of DNA lesions. The activity of these factors in cells is controlled by a complex network of post-translational modifications (PTMs). However, the role of epigenetic PTMs in controlling the DRR is less well understood. This is especially true in neuronal cells, which rely on specialised DDR sub-pathways for repair of damage, whilst at the same time being more prone to damage as a consequence of high metabolic activity. My group is interested in one particular PTM, lysine methylation, the enzymes that catalyse this, and how they control the DDR in neurons. Studies from our lab (amongst others) have shown that these ‘lysine methyltransferases’ play vital roles in promoting DNA repair via several DDR pathways, as well as maintaining neurological function. Indeed, cells from patients deficient in lysine methylation enzymes exhibit defects in the DDR as well as neurological diseases. However, it is unclear whether the neurological phenotypes seen in these patients arise because of defective DNA repair. This PhD will investigate how loss of lysine methylation impacts upon the DDR in neurons and investigate the consequences for neuronal function. The project will involve a wide variety of laboratory techniques, including culture of iPSC and neuronal cells, co-immunoprecipitation, CRISPR-Cas9 and Cas12 techniques, in vitro activity and binding assays, fluorescent and visual microscopy, immunoblotting and immunofluorescence, molecular cloning, and metabolic/neuronal activity assays. These approaches will lead to a greater understanding of how lysine methylation is involved in maintaining genome stability in neurons and the implications for neurological disease. For further information, please contact m.r.higgs@bham.ac.uk. Person Specification: Applicants should have a strong background in molecular and cellular biology, with experience of the following laboratory techniques: cell culture, immunofluorescence; immunoblotting and molecular cloning. Previous experience of a research lab environment and mammalian tissue culture is essential. They should be ambitious, enthusiastic and self-motivated, and hold at least an Upper Second Class Honours Degree in a relevant biological subject. If applicable, they should also be able to demonstrate proficiency in the English language with relevant scores in both reading and speaking (e.g. IELTS). Funding Notes Self-funded PhD students only. References H3K4 methylation by SETD1A/BOD1L facilitates RIF1-dependent NHEJ. Bayley et al. Mol Cell. 2022 82(10):1924-1939.e10.Histone methylation by SETD1A protects nascent DNA through the nucleosome chaperone activity of FANCD2. Higgs et al. Mol Cell 2018 71(1):25-41.Characterization of SETD1A haploinsufficiency in humans and Drosophila defines a novel neurodevelopmental syndrome. Kummeling et al. Mol Psych 2020: in press. doi: 10.1038/s41380-020-0725-5.Hijacked in cancer: the KMT2 (MLL) family of methyltransferases. Rao and Dou. Nature Reviews Cancer 2015 15; 334-346.Chromatin modification and remodeling in schizophrenia. Duan. In Translational Epigenetics, Chromatin Signaling and Neurological Disorders. 2019 Volume 12; 303-330. doi: 10.1016/B978-0-12-813796-3.00014-6. Apply Now

 Prof Alicia Hidalgo Application Deadline: Applications accepted all year round Details The aim is to discover and test candidate molecular mechanisms underlying how the central nervous system (CNS) (ie spinal cord and brain) responds to life challenges, for example life experience or injury, driving plasticity, regeneration or degeneration. We aim to understand why distinct experiences result in adaptation through learning, whilst others can lead to unsurmountable stress, psychiatric and behavioural disorders. We will test the hypothesis that experience results in structural modifications to cells that alter neural circuit connectivity patterns that in turn modify behaviour. Synapses and changes in cell shape are made and unmade every day, as we go about our lives. And if cells change, connectivity patterns in the brain change: what are the consequences to behaviour, what we do, how we feel? The brain is plastic: structural plasticity enable us to form new synapses and connectivity patterns as we learn and adapt to life challenges, encoding memory. Structural homeostasis constrains the brain’s ability to change, thus maintaining neural circuits stable. Exercise and learning increase structural plasticity, whilst homeostatic meachanism can lead to degeneration underlying neurodegenerative diseases (e.g. Alzheimer’s and Parkinson’s), neuro-inflammation and psychiatric disorders (e.g. depression). The cellular processes underlying structural brain change include neurogenesis and gliogenesis, cell loss, changes in cell shape, synapse formation and loss, modifying circuits an behaviour. As behaviour is a source of experience, we aim to find out how cycles of experience and behaviour modify our brain throughout life. On the other hand, the human central nervous system does not regenerate after injury (for example to the spinal cord) or disease. Injury triggers an inflammatory reaction leading to further cell loss. However, some animals can regenerate their CNS. Furthermore, the human brain is plastic, meaning it can undergo change, enabling neurogenesis, gliogenesis, formation of new synapses and connections in response to challenges. This means that regeneration of cells and connections in the spinal cord or brain after damage could be possible. Animals that can regenerate their CNS do so by inducing de novo neurogenesis followed by integration of new neurons into functional neural circuits. In humans, new neurons are made daily during learning, and these new neurons also integrate into functional circuits. This means that cells can ‘know’ how to re-establish cell populations and circuits. It may possible to tap into the regenerative potential of the CNS to direct regeneration after injury and damage. We will use the fruit-fly Drosophila as a model organism, for its unparalleled, powerful genetics. We will investigate the molecular and cellular mechanisms that drive inflammatory and degenerative responses versus plastic and regenerative responses to life experience or injury. The approach will combine a wide range of techniques including: advanced genetics to manipulate genes and cells, molecular cell biology including CRISPR/Cas9 gene editing technology and transgenesis, microscopy, including laser scanning confocal microscopy and calcium imaging in time-lapse, computational imaging approaches for analysis of images and movie recordings, analysis of the connectome to identify neural circuits, stimulating neuronal function with opto- and thermo-genetics in vivo, recording and analysing fruit-fly behaviour, aided by computational data analyses tools. Funding Notes This project is open to any student. Self-funded students (e.g. who could access studentships from their own crountry) are invited to apply. Apply Now

Prof G Stewart Application Deadline: Applications accepted all year round Details Defective DNA repair is a major driver of genetic instability and cancer development. This PhD project, based in Professor Stewart’s laboratory, will investigate how cells detect and repair DNA damage, and how defects in these processes give rise to human disease. By studying rare inherited disorders, the project aims to generate fundamental insights into the DNA damage response and its role in conditions such as neurodegeneration, developmental abnormalities, immune dysfunction, infertility, and cancer. Research Focus: The Stewart laboratory has extensive expertise in the molecular characterisation of rare genetic disorders associated with defective DNA repair and abnormal DNA replication, including Ataxia-Telangiectasia, Fanconi Anaemia, Seckel Syndrome, and Microcephalic Primordial Dwarfism. Building on this work, the project will focus on newly identified inherited syndromes linked to genome instability, arising from defects in DNA replication, replication stress responses, or specific DNA repair pathways. Using patient-derived cell models and state-of-the-art molecular and cellular biology techniques, you will define how specific gene variants disrupt genome maintenance and drive disease. This will involve a combination of genetic, biochemical, and cell biology approaches, offering comprehensive training in cutting-edge research methods. Training and Impact: This project provides an excellent opportunity to gain expertise in genome stability, human genetics, and disease mechanisms within a collaborative and translational research environment. Findings from this work will not only contribute to improved genetic diagnosis, clinical management, and counselling for patients, but may also identify novel cellular pathways and targets relevant to more common diseases, including cancer. Funding Notes Self-funding must include a reasonable level of costs to cover yearly laboratory bench fees. References References:1. Reynolds JJ, Bicknell LS, Carroll P, Higgs MR, Shaheen R, Murray JE, Papadopoulos DK, Leitch A, Murina O, Tarnauskaitė Ž, Wessel SR, Zlatanou A, Vernet A, Kriegsheim A, Mottram RMA, Logan CV, Bye H, Li Y, Brean A, Maddirevula S, Challis RC, Skouloudaki K, Almoisheer A, Alsaif HS, Amar A, Prescott NJ, Bober MB, Duker A, Faqeih E, Seidahmed MZ, Tala SA, Alswaid A, Ahmed S, Al-Aama JY, Altmüller J, Balwi MA, Brady AF, Chessa L, Cox H, Fischetto R, Heller R, Henderson BD, Hobson E, Nürnberg P, Percin EF, Peron S, Spaccini L, Quigley AJ, Thakur S, Wise CA, Yoon G, Alnemer M, Tomancak P, Yigit G, Taylor AMR, Reijns MAM, Simpson MA, Cortez D, Alkuraya FS, Mathew CG, Jackson AP, Stewart GS. (2017). Mutations in DONSON disrupt replication fork stability and cause microcephalic dwarfism. Nature Genet. 49:537-5492. Baxley RM, Leung W, Schmit MM, Matson JP, Oram MK, Wang L, Yin L, Hedberg J, Rogers CB, Harvey AJ, Basu D, Hendrickson EA, Mace EM, Orange JS, Aihara H, Stewart GS, Blair E, Gowen Cook J, Bielinsky AK. (2020). Bi-allelic MCM10 mutations cause telomere shortening with immune dysfunction and cardiomyopathy. Nature Commun. 12:16263. Abu-Libdeh B, Jhujh SS, Dhar S, Sommers JA, Datta A, Longo GMC, Grange LJ, Reynolds JJ, Cooke SL, McNee GS, Hollingworth R, Woodward BL, Ganesh AN, Smerdon SJ, Nicolae CM, Durlacher-Betzer K, Molho-Pessach V, Abu-Libdeh A, Meiner V, Moldovan G-L, Roukos V, Harel T, Brosh Jr. RM, Stewart GS. (2022). RECON Syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1. J Clin Invest. 132:e1473014. Grange LJ, Reynolds JJ, Ullah F, Isidor B, Shearer RF, Latypova X, Baxley RM, Oliver AW, Ganesh AN, Cooke SL, Jhujh SS, McNee GS, Hollingworth R, Higgs MR, Natsume T, Khan T, Martos-Moreno GÁ, Chupp S, Mathew CG, Parry D, Simpson MA, Nahavandi N, Yüksel Z, Drasdo M, Kron A, Vogt P, Jonasson A, Seth SA, Gonzaga-Jauregui C, Brigatti KW, Stegmann APA, Kanemaki M, Josifova D, Uchiyama Y, Oh Y, Morimoto A, Osaka H, Ammous Z, Argente J, Matsumoto N, Stumpel CTRM, Taylor AMR, Jackson AP, Bielinsky A-K, Mailand N, Le Caignec C, Davis EE, Stewart GS. (2022). Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy. Nature Commun. 13:66645. Woodward BL, Lahiri S, Chauhan AS, Garcia MR, Goodley L, Clarke TL, Pal M, Agathanggelou A, Jhujh SS, Ganesh AN, Hollins, FM, Galassi Defore V, Maroofian R, Efthymiou S, Meinhardt A, Mathew CG, Simpson MA, Mefford HC, Faqeih EA, Rosenweig SD, Volpi S, Di Matteo G, Cancrini C, Scardamaglia A, Shackley F, Davies EG, Ibrahim S, Arkwright P, Zaki MS, Stankovic T, Taylor AMR, Mazur AJ, Di Donato N, Houlden H, Rothenberg E, Stewart GS. (2025). Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by -actin. Nature Commun. 16:4491 Apply Now

 Dr Rasha Abu-Eid Application Deadline: Applications accepted all year round Details The incidence of head and neck cancer (HNC) is on the rise globally. Despite advances in HNC treatment and diagnosis, the mortality rate is high. This is mainly attributed to late diagnosis of established malignancies and the absence of reliable biomarkers for predicting malignant transformation in oral potentially malignant disorders, which carry a higher risk of malignant transformation. The identification of biomarkers for screening and early detection of disease progression is crucial. Salivary biomarkers are showing promise as diagnostic and prognostic markers for disease progression. Many of these biomarkers are expressed in extracellular vesicles that are shed from different cells in the oral environment. In addition to their potential use as biomarkers capable of predicting disease progression, extracellular vesicles can modulate the immune system within the tumour microenvironment, thus affecting patient outcome. This project aims at characterising the properties of HNC cell line derived extracellular vesicles and assessing their role in keratinocyte and immune cell function. This is an exciting project that provides the student with opportunities to use cutting edge technologies including flow cytometry, light and electron microscopy, image analysis, cell culture, FTIR and Raman spectroscopy in addition to gaining in depth knowledge of oral cancer pathogenesis, disease progression and extracellular vesicle biology. Apply Now