University of Dundee, Scotland, United Kingdom invites online Application for number of Funded PhD Opportunities in various Departments. We are providing a list of Fully Funded Doctoral Research Positions available at University of Dundee, Scotland, United Kingdom.
Eligible candidate may Apply as soon as possible.
(01) Funded PhD Opportunities
Summary/title: Destroying cancer-causing proteins
This PhD project will explore precisely how FAM83D, FAM83F, and FAM83G regulate cell division and cancer cell proliferation, with a particular focus on their degradation as a therapeutic strategy. The project will employ a wide range of multi-disciplinary cutting-edge technologies, such as CRISPR/Cas9 genome editing, mass-spectrometry, DEL screens to identify ligands for FAM83D, FAM83F and FAM83G, and development and application of small molecule degraders, including PROTACs and molecular glues, against FAM83D-CK1-alpha, FAM83F-CK1-alpha and FAM83G-CK1-alpha complexes. The aim is to establish a mechanistic foundation and therapeutic rationale for selectively degrading these proteins complexes to suppress cancer cell growth.
Closing date : 31 January 2026
(02) Funded PhD Opportunities
Summary/title: Decoding the mechanism and function of ER-Ribosome associated Quality Control
Approximately one third of the human proteome depends on the endoplasmic reticulum (ER) for its biosynthesis. During translation, ribosomes can sometimes stall, triggering a chain of events that results in the decay of defective mRNAs, recycling of stalled ribosomes and crucially, degradation of partially synthesized nascent polypeptides. UFM1 is an enigmatic ubiquitin-like modifier that is attached to ER-associated ribosomes when stalling occurs. The role of this UFM1 attachment is not fully understood, but mutations in the UFM1 pathway have been found in several neurodevelopmental disorders, emphasizing its significance.
The goal of this project is to define how ribosomes get UFMylated upon stalling and to investigate the mechanisms and function of ribosome UFMylation. This project will build on our recent unpublished work, and we are looking for curious and creative students to work at the frontier of an exciting new field. What makes this project especially exciting is its potential to reveal a fundamental pathway responsible for quality control and homeostasis at the ER, the disruption of which causes disease.
Closing date : 31 January 2026
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(03) Funded PhD Opportunities
Summary/title: Decoding the hidden language of ubiquitin: non-canonical ubiquitylation in human health and disease
Ubiquitylation is one of the cell’s most powerful control switches, fine-tuning everything, from protein stability to gene expression. When this system malfunctions, it fuels diseases including cancer, neurodegeneration and immunity disorders. This PhD project will focus on exploring non-canonical ubiquitylation – a paradigm-shifting discovery where ubiquitin tags not just lysine residues on proteins but also serine, threonine, DNA, RNA, and sugars. Decoding this hidden molecular “language” of ubiquitin could transform our understanding of cell regulation and uncover untapped therapeutic possibilities.
Recent work in the De Cesare lab has identified the UBE2Q family of ubiquitin-conjugating enzymes (UBE2Q1, UBE2Q2, and UBE2QL1) as key mediators of non-canonical ubiquitylation[1]. These enzymes are linked to vital processes such as lysophagy and embryo implantation and are dysregulated in cancer and neuronal apoptosis – pointing to a widespread but hidden role in human health and disease.
As the PhD candidate, you will:
- Define the biological functions of the UBE2Q enzyme family, identifying and validating their substrates, and uncovering novel disease pathways and therapeutic targets.
- Map non-canonical ubiquitylation events at a proteome-wide scale using cutting-edge quantitative proteomics.
- Dissect molecular mechanisms using a multidisciplinary toolkit: structural biology, molecular and cell biology, protein biochemistry, and biophysics.
Closing date : 31 January 2026
(04) Funded PhD Opportunities
Summary/title: Decoding a New Signalling Axis in Parkinson’s Disease
You will investigate how disrupting the TMEM55B–RILPL1 axis impacts lysosomal biology and Parkinson’s disease -relevant signalling. Using brain tissue and primary cells from these mouse models, you will perform lysosome immunoprecipitations (Lyso-IPs) followed by deep proteomic, lipidomic, and phosphoproteomic profiling using advanced mass spectrometry. You will analyse multi-omics datasets to map signalling changes, identify key effectors, and validate them through mechanistic cell biology experiments.
Closing date : 31 January 2026
(05) Funded PhD Opportunities
Summary/title: Deciphering novel ALS signalling pathways: Biomarker discovery and developing therapeutic strategies
Motor neuron disease also referred as Amyotrophic lateral sclerosis (ALS) is a rapidly progressive debilitating disease affecting upper and lower motor neurons with a median survival rate of 2-3 years. Currently, riluzole that extends survival by only 2-3 months, is the only globally approved drug. The well studied ALS genes include TDP-43, an RNA-binding protein localised within nucleus that regulate splicing and RNA metabolism. Loss of function (LoF) of TDP-43 leads nuclear mis-localisation and cytoplasmic aggregation which is a hallmark of 97% of ALS cases and indeed observed in other neurogenerative diseases such as FTD and Alzheimer’s. LoF TDP-43 leads to the generation of several cryptic exons on plethora of genes and have been observed to be denovo translated leading to non-functional protein products and may affect their natural function and altered signalling cascades (1). There is an unmet need to better understand the pathways and molecular consequences of loss of function (LoF) and gain of toxicity of TDP-43 in neuronal and glial cells which collectively has been implicated as a key feature of TDP-43 proteinopathies.
A PhD project is available to develop a knowledgebase of TDP-43 loss of function (LoF) mediated cryptic splicing, identification of cryptic peptides, development of ultra-sensitive assays for mechanistic understanding TDP-43 LoF biology.
Closing date : 31 January 2026
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(06) Funded PhD Opportunities
Summary/title: Structural and Chemical Biology of Ubiquitin E3 Ligases
The covalent attachment of the small protein ubiquitin to substrates regulates virtually all cellular processes, and its modulation with small molecules is poised to revolutionise modern medicine. Central to the ubiquitin system are E3 ligase enzymes, which catalyse the covalent transfer of ubiquitin to specific substrates.
Our multidisciplinary lab has developed pioneering technologies for E3 ligase discovery and activity measurement 1,2. Using these approaches, we have identified several E3 ligases with unconventional transfer and regulatory mechanisms 2-5. For example, MYCBP2, a member of the RING-Cys-relay (RCR) subtype, is a central regulator of neuronal integrity 2,3. We have also characterised RNF213-ZNFX1 (RZ-type) E3 ligases, which confer innate restriction to microbial pathogens. Their distinct ubiquitin transfer mechanisms and remarkable regulatory interplay with nucleotide- and nucleic acid–binding domains unlocks novel ways of therapeutically modulating E3 activity.
Key to advancing both our understanding of these mechanisms and the development of new therapies is the atomic-level characterisation of their molecular functions. Equally crucial is developing new technologies for interrogating E3 activity in cells.
Closing date : 31 January 2026
(07) Funded PhD Opportunities
Summary/title: Viral interference of ISG15 signals
One of the most important challenges facing biomedical research is to understand the molecular details of how our immune system defends against pathogens. In the Swatek lab, we aim to understand the roles of ubiquitin and ubiquitin-like modifications in the antiviral state (1). These modifications have emerged as crucial mediators of the signal transduction pathways that sense and respond to viruses. The ubiquitin-like protein, ISG15, is highly upregulated during viral infection and marks thousands of proteins to help shape the host defence response. To subvert ISG15 signalling, many viruses encode enzymes that remove these modifications, and we have previously identified an elegant example of viral-mediated ISG15 suppression (2). Surprisingly, however, the roles of the vast majority of ISG15 modifications are unknown, and therefore, understanding how ISG15 contributes to the antiviral state is of paramount importance. This PhD project aims to identify the ISG15 substrates targeted by viral effector proteins and link these discoveries to a cellular function.
This project takes advantage of our expansive toolkit to study the ISG15 system. Students interested in gaining expertise in a wide variety of approaches are strongly encouraged to apply since the project merges several disciplines, including method development, state-of-the-art mass spectrometry, cell biology, structural biology, biophysics, and biochemistry (3-4). The student will have the opportunity to participate in several internal and external collaborations.
Closing date : 31 January 2026
(08) Funded PhD Opportunities
Summary/title: Unravelling the molecular mechanisms of amyotrophic lateral sclerosis/motor neuron disease
Amyotrophic lateral sclerosis (ALS)—the commonest type of motor neuron disease (MND)—is a rapidly progressive paralysing illness of mid-adulthood. It has a lifetime risk of ~1 in 400, resulting from the selective neurodegeneration of upper and lower motor neurons (MNs). ~10% of ALS is inherited, and the rest occurs spontaneously. The median survival from symptom onset is 3 years and there are no significant treatments, and no cure. The only globally licensed medication, Riluzole, prolongs survival by a few months on average, and was introduced in the mid 1990s. Consequently, there is a major impetus to unravel the key molecular pathomechanisms to make a breakthrough.
To date, mutations in >40 genes have been identified as a cause of familial ALS/MND that have significantly advanced our understanding of the pathogenesis. Several encode or could interact with protein kinases, implicating dysregulation of protein phosphorylation in ALS pathogenesis, although a single coherent signalling pathway that explains MN degeneration remains elusive.
Closing date : 31 January 2026
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(09) Funded PhD Opportunities
Summary/title: Crosstalk between UPR Signaling and ER-phagy during ER Stress
The endoplasmic reticulum (ER) plays a central role in protein folding, modification, and secretion. Perturbations in these processes trigger ER stress and activate the unfolded protein response (UPR), a signaling network that aims to restore ER homeostasis. Dysregulation of ER homeostasis contributes to a wide range of pathologies, including cancer, tissue fibrosis, metabolic disorders, and neurodevelopmental defects. ER quality control is also maintained by the proteasome (via ER-associated degradation, ERAD) and the autolysosome (via ER-specific autophagy, ER-phagy)1-3. Together, the UPR, ERAD, and ER-phagy coordinate ER quality control to safeguard cellular function.
Whereas the UPR is canonically known to activate ERAD, our recent unpublished data indicate that UPR signaling represses ER-phagy activity. This observation has strong implications for autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, where antibody hyperproduction drives chronic ER stress and aberrant UPR activation. We hypothesize that the UPR–ER-phagy axis could represent a therapeutic target, enabling rerouting of excess antibody cargo towards autophagic degradation rather than secretion.
The aim of this PhD project is to elucidate the molecular mechanisms by which UPR signaling regulates ER-phagy and to investigate the physiological relevance of this crosstalk in autoimmune disease models. The project will employ disease-relevant immune cell systems to explore the feasibility of activating ER-phagy to promote degradation of ER proteins, including misfolded aggregates and antibodies.
Closing date : 31 January 2026
(10) Funded PhD Opportunities
Summary/title: Cleave to Modify: A new biological mechanism for protein regulation
This PhD project aims to identify novel substrates and pathways regulated by the “cleave-to-modify” mechanism and link these discoveries to cellular function. By doing so, the project will provide fundamental insights into how proteolytic processing diversifies protein function and reveal new opportunities for therapeutic intervention.
This project takes advantage of our recently developed toolkit to study UBL fusion proteins and their processing4. Students interested in gaining expertise in a wide variety of approaches are strongly encouraged to apply, since the project merges several disciplines, including: method development, state-of-the-art mass spectrometry, cell biology, biophysics, and biochemistry.
Closing date : 31 January 2026
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(11) Funded PhD Opportunities
Summary/title: New technologies to monitor assembly of alternative forms of the proteasome
The PhD project aims to engineer the proteasome and develop new technologies to monitor the assembly of its alternative forms, in a format suitable for high-throughput screening. These tools will be instrumental in uncovering the functions of alternative proteasome complexes and in clarifying their involvement in disease. For example, mutations in proteasome subunits cause proteasomopathies (juvenile neurodevelopmental disorders), while mutations in proteasome-associated proteins are linked to early-onset Parkinson’s disease. Ultimately, this work will lay the foundation for novel strategies to restore protein homeostasis in neurodegenerative disorders. The project will offer training opportunities in state-of-the-art technologies such as cell engineering (CRISPR-Cas9 gene editing of proteasome genes), molecular biology (proteasome and protein degradation assays), and high-resolution confocal microscopy (proteasome dynamics).
Closing date : 31 January 2026
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(12) Funded PhD Opportunities
Summary/title: Investigating the immune-epithelial interactions that drive intestinal inflammation
Intraepithelial T lymphocytes (IELs) are at the forefront of mucosal immunity – the first immune cells that pathogens and symbionts encounter in the gut. IELs are central to the protection of the gut against infection and dietary stress, but dysregulated IELs responses are also associated with autoimmune inflammatory bowel diseases such as Coeliac and Crohn’s disease. Importantly, these unique T cells reside between nutrient-absorptive intestinal epithelial cells, close to the anaerobic microbes in the intestinal lumen. How IELs are able to respond to changes in intestinal epithelial cells and how they influence nutrition absorption and epithelial defence is currently unclear (1).
The aim of this project is to investigate how specific molecular regulators in IELs allows them to adapt to the intestinal microenvironment and mount appropriate responses to intestinal perturbations, including diet and microbial challenges. The discovery that PIM kinases uniquely regulate metabolic activation of IEL (2), and that T-cell receptor signalling in IEL is uniquely modified (3) , and that IEL have a unique metabolic signature (4), all suggest that changes in these molecular components are necessary for IELs to function. In this project, the student will learn to use state-of-the-art techniques including proteomics and phosphoproteomics, Ribo-Seq to rapidly identify changes in IEL, and in vivo models to address how perturbations in signalling pathways regulate intestinal homeostasis.
Closing date : 31 January 2026
(13) Funded PhD Opportunities
Summary/title: How do Dysregulated Signalling Pathways cause Intellectual Disability?
The goal of our lab is to understand how signal transduction is disrupted to cause intellectual disability, which is a major healthcare challenge world-wide. Recent data indicates that genes encoding signalling enzymes such as protein kinases are frequently mutated in intellectual disability, suggesting that these components may form novel signalling pathways which are required for neurological functioning and are disrupted in patients (1). We recently discovered the first example of such a pathway, comprising Ser-Arg Protein Kinase (SRPK)(2) and the RNF12/RLIM E3 ubiquitin ligase (3,4), which controls neurodevelopmental processes and is disrupted by intellectual disability gene variants (5,6).
This PhD project aims to map signalling pathways that are disrupted in intellectual disability, with the overarching goal of uncovering much-needed therapeutic opportunities in this area. The successful candidate will have the opportunity to utilise exciting new tools and reagents in the lab and expand on our recent progress in dissecting intellectual disability signalling networks. Potential approaches include (phospho)proteomic profiling mass-spectrometry, modelling human neural development using pluripotent stem cells, animal models of intellectual disability, cutting edge biochemistry, and structural analysis using Cryogenic Electron Microscopy (CryoEM). The student will be embedded in a dynamic team with a track record in dissecting intellectual disability signalling networks. They will also have excellent opportunities for further internal and external collaborations with leading experts in this area.
Closing date : 31 January 2026
(14) Funded PhD Opportunities
Summary/title: Genome Bodyguards: Investigating the Cell’s Hidden Repair Team
The MMS22L–TONSL complex is a molecular “first responder” that helps cells protect and repair their DNA when it gets damaged during everyday life. In fact, when we use genome-editing to switch off this complex, cells die within one cell division. The problem is that without it, cells struggle to maintain the integrity of their genetic material—a problem at the heart of cancer, ageing, and many inherited diseases. Actually, TONSL overexpression has been linked to a range of cancers, and mutation in this gene cause debilitating symptoms. A major issue this that we don’t know how MMS22L-TONSL works at the molecular level. This state-of-the-art PhD project will explore how this complex works at the molecular level, discovering how it recognizes broken DNA, recruits repair machinery, and safeguards the stability of the genome. The project you’ll be part of is a collaboration with leading experts in genome maintenance around the world. By combining cutting-edge biochemistry, molecular biology, structural studies, and live-cell imaging, as well as genome-editing and genome-wide “-omic” technologies, the project aims to uncover new exciting insights into how cells defend themselves and how these processes can be harnessed in medicine.
Closing date : 31 January 2026
(15) Funded PhD Opportunities
Summary/title: From Data to Biology: AI-Driven Biomarker Discovery and Validation in Parkinson’s Disease through the MJFF LITE Initiative
This PhD studentship is embedded within the translational pillar of the Michael J. Fox Foundation–funded LRRK2 Investigative Therapeutic Exchange (LITE) initiative – a landmark international collaboration designed to accelerate the development of LRRK2-targeted therapies and biomarkers. The LITE study offers an unprecedented cohort of deeply phenotyped LRRK2 mutation carriers and related loci, with exceptional biosample depth that includes clinical and imaging phenotyping, genetic data, and mass spectrometry–based profiling of urine and plasma. Critically, LITE also incorporates innovative “tagless” lysosomal immunoprecipitations (LysoIP), enabling immuno enrichment of lysosomes for multimodal mass spectrometry profiling of proteins, lipids, and metabolites (PMID: 39724071). This combination of clinical depth and molecular resolution provides a unique opportunity to uncover robust biological signatures of LRRK2 dysfunction.
Closing date : 31 January 2026
(16) Funded PhD Opportunities
Summary/title: Finding the eat-me signals
The Ganley lab is interested in unravelling the molecular mechanism of autophagy (which literally translates from the Greek meaning to eat oneself). Autophagy is a critical lysosomal degradation pathway that functions to clear the cell of potentially damaging agents, such as protein aggregates or faulty mitochondria. Importantly, autophagy appears to be dysregulated in many diseases and therefore its modulation could lead to novel therapies. However, to enable this, we first need to understand the machinery involved.
A project is available to decipher the signals that lead to the specific autophagy of mitochondria (termed mitophagy), a process that has strong links to cancer and in particular Parkinson’s disease. Following up on recently published work, the project will utilise state-of-the-art microscopy, cell biology, protein biochemistry and mass spectrometry to identify phosphorylation and ubiquitylation events involved in capturing mitochondria for degradation. As well as gaining experience in a wide variety of techniques, you will be part of a dynamic and collaborative team intent on making new scientific discoveries and producing the next generation of world-class scientists.
Closing date : 31 January 2026
(17) Funded PhD Opportunities
Summary/title: Discovery of novel organelle and ubiquitin mechanisms underlying Parkinson’s disease
Parkinson’s disease (PD) is a movement disorder that is now the fastest growing neurological disorder in the world. Despite much research the disease is incurable and there are no treatments that can slow the disease down. The discovery of genetic mutations in rare familial forms has transformed our understanding of the origins of PD but the function of these genes is poorly understood. Mutations in PTEN-induced kinase 1 (PINK1) cause autosomal recessive PD. PINK1 is unique amongst all protein kinases due to the presence of a mitochondrial targeting domain that localises it to mitochondria. Our lab has made a number of groundbreaking discoveries and uncovered mechanisms that explain how PINK1 and Parkin activation lead to the removal of damaged mitochondria by mitophagy. Excitingly based on this research there are now Phase I trials for PD patients using molecules that boost PINK1-dependent mitophagy. However, there remain many outstanding questions on the regulation of PINK1 and its downstream biology that may lead to new diagnostic and therapeutic strategies to tackle PD. These include the molecular mechanism by which PINK1 senses mitochondrial damage; the role of other PINK1 substrates including Rab GTPases; how PINK1 mutations impacts other organelles including lysosomes and endosomes;; and identification of ubiquitin regulators of PINK1 dependent mechanisms. Our lab uses a multidisciplinary approach to address these questions and the successful student will gain exposure and training in many state-of-the-art methods including mass spectrometry / proteomic technologies; CRISPR/Cas9 technologies; cutting edge methods to isolate organelles, and tissue culture using human iPSC-derived neurons or mice-based analysis. The lab also collaborates with many labs around the world and is actively involved in public engagement. In addition to training and development opportunities within the MRC Protein Phosphorylation & Ubiquitylation Unit and Dundee , the Muqit lab is a member of the EMBO Young Investigator Network (https://people.embo.org/profile/miratul-muqit) and students have opportunities to attend EMBO PhD courses and workshops. The lab is also part of the innovative global Aligning Science Across Parkinson’s (ASAP) initiative (https://parkinsonsroadmap.org) that also enables students to experience cutting edge development opportunities.
Closing date : 31 January 2026
(18) Funded PhD Opportunities
Summary/title: Evaluation of the neuroprotective actions of adiponectin in dementia
Appropriate communication between brain cells determines how we think and behave. In Alzheimer’s disease (AD), communication between brain cells is impaired, resulting in memory deficits. AD-related memory deficits are linked to the build-up of a protein called tau, which ultimately inhibits communication between brain cells. Consequently, identifying agents that limit tau build-up and prevent its unwanted effects on brain cell communication is likely to be beneficial in AD.
Adiponectin is a metabolic hormone secreted by fat cells that readily accesses the brain and can influence important brain functions. Recent studies suggest that adiponectin has therapeutic benefits as it reverses memory deficits in rodent models of AD. But the protective effects of adiponectin and its effects on tau build up, and brain cell communication are unclear. Here, we propose to address this key gap in our knowledge. We will assess the neuroprotective actions of adiponectin using various cellular and animal models that replicate the unwanted effects of tau protein that occur in AD. Additionally, we will evaluate the cell signalling pathways that are key to adiponectin’s protective actions. This will increase our understanding of the brain effects of adiponectin and provide valuable information on the therapeutic potential of adiponectin in AD.
Closing date : 9 January 2026
(19) Funded PhD Opportunities
Summary/title: The role of accounting in prefiguring regenerative organising – an exploration of grassroots urban and nature-based innovation
Drawing on research in accounting innovations, this project explores the role of prefigurative accounting to realise, reconfigure, operationalise and scale up principles of regenerative sustainability. The project contributes to the themes of nature and place-based innovation by exploring the role of accounting in prefiguring authentic regenerative practice. Our empirical focus will be on participatory, non-hierarchical, and ecologically sustainable practices at a grassroots level in Scotland. The project aims to explore the interactions between financing institutions and communities of transformation who are acting as if they are already present in a regenerative future based on alternative practices and governance principles. This will involve urban as well as nature-based regeneration cases. Rather than concentrating on existing high-profile and large-scale settings, the project will instead seek to engage with actors on the margins of regenerative innovation in Scotland, involved in projects at a grassroots level, where authentic prefigurative innovation is most likely to be found.
Closing date : 9 January 2026
(20) Funded PhD Opportunities
Summary/title: Regenerating rivers – flow physics informed tracking and removal of microplastics in rivers
The aims of this proposal are to develop a model to understand the long-term distribution of microplastics (MPs), validate the model via a Citizen Science campaign, and to identify MP hotspots to inform regenerative interventions.
Closing date : 9 January 2026
(21) Funded PhD Opportunities
Summary/title: Police, communities and the climate crisis
This project aims to develop a regenerative and equitable approach to oral health monitoring using non-invasive optical coherence imaging (OCT/OCTA). It seeks to replace invasive, resource-intensive diagnostics such as biopsy with a sustainable, community-based model of preventive care. The research focuses on advancing light-based imaging to regenerate diagnostic capability in underserved settings, while reducing environmental and material waste.
The overall aim of the project is to investigate Police, Communities and the Climate Crisis through a place-based approach.
There are three primary objectives:
- Assessing the current levels of preparedness in policing and local authority agencies for extreme weather-related crime events in three case study areas.
- Assessing community experiences of extreme weather-related crime events in three case study areas.
- Developing a model of epistocratic co-production to build local resilience to extreme weather-related crime events and testing this in three case study areas.
Closing date : 9 January 2026
(22) Funded PhD Opportunities
Summary/title: Non-invasive optical imaging for oral health – regenerative innovation towards a restorative and equitable health system
This project aims to develop a regenerative and equitable approach to oral health monitoring using non-invasive optical coherence imaging (OCT/OCTA). It seeks to replace invasive, resource-intensive diagnostics such as biopsy with a sustainable, community-based model of preventive care. The research focuses on advancing light-based imaging to regenerate diagnostic capability in underserved settings, while reducing environmental and material waste.
Closing date :9 January 2026
(23) Funded PhD Opportunities
Summary/title: New-Eden-Tay – Nature-based innovations for adaptation, resilience and restoration of the watersheds of Eden and Tay Rivers in a changing climate
The New-Eden-Tay project aims to explore nature-based and place-based innovations for adaptation, resilience, and restoration within the Eden and Tay watersheds in a changing climate. The project will advance the integration of existing future climate projections, high-resolution hydrological modelling of the region, nature-based innovations and two-way stakeholder engagement. The combination of environmental and human dimensions within our modelling, analysis, and communication framework will enable reduction of the flood and drought risks, enhance ecosystem restoration and disaster resilience, and provide a climate-positive human experience.
Closing date : 9 January 2026
(24) Funded PhD Opportunities
Summary/title: Future health and social care systems: regenerating healthcare pathways for equitable health and wellbeing
- Explore possible futures of health/care pathways that respond to demographic shifts and the increasing prevalence of chronic/degenerative conditions.
- Reimagine health/care systems through the lens of regenerative innovation, exploring how they might restore wellbeing, renew trust and promote equity within contexts such as ageing, chronic illness or substance use service.
- Identify how intersecting characteristics (e.g., age, ethnicity/race, gender, disability, migration status) shape experiences of health inequity across different future scenarios.
- Co-create regenerative models of health/care that move beyond adaptation to active restoration of health, wellbeing, community connection and environmental balance.
Closing date : 9 January 2026
(25) Funded PhD Opportunities
Summary/title: Discovering novel catalysts for carbon capture and green hydrogen production for climate resilience
In this project, we aim to predict novel metal-organic frameworks (MOFs), awarded the Nobel Prize in Chemistry in 2025, for use as catalysts in Carbon Capture and hydrogen production. MOFs are porous, crystalline materials made of metal ions and organic linker molecules, forming an open grid-like structure with high surface area and tunable pore size. These properties make them ideal for gas storage and catalysis.
The work will be divided into four work packages:
- Predict with Density functional theory (DFT) the structure of novel MOFs with large pores for CO2 capture and synthesise them in collaboration with experimental groups.
- Demonstrate the action of MOFs in CO2 capture using MD+MLIP and contribute to understanding experimental characterisation.
- Further search for large surface area MOFs for photo-electrocatalysis of water to yield H2.
- Demonstrate photo-electrocatalytic action on the large surface area of MOFs using MD+MLIP and experimental catalysis.
Closing date : 9 January 2026
(26) Funded PhD Opportunities
Summary/title: Designing regenerative futures: empowering young people through craft practice and place-based innovation (in Dundee)
This PhD aims to explore how regenerative design, grounded in participatory craft practice and material-led making, can address social isolation among young people aged 16-25 in Dundee. It develops and tests a regenerative design framework and toolkit empowering young people to co-create regenerative futures through place-based innovation, collective skill-building, and imaginative engagement with natural, reclaimed, and locally sourced materials.
Closing date : 9 January 2026
(27) Funded PhD Opportunities
Summary/title: CRAFT – Co-designed Regenerative AI Flow Country Toolkit: credible, fast decision support for peatland rewetting
This project develops AI surrogates to optimise peatland regeneration across multiple objectives, such as carbon sequestration, biodiversity habitat, wildfire risk reduction, flood attenuation, and community benefits, using a place-based, co-designed approach. Uniquely, the project will translate place-based knowledge into the surrogate itself through co-design with domain scientists and stakeholders so that diverse views shape model design and interfaces, aligning with “Doing AI Differently” (Hemment et al. 2025).
Closing date : 9 January 2026
(28) Funded PhD Opportunities
Summary/title: Co-designing regenerative therapeutic spaces
Place, environment, and nature profoundly shape human wellbeing and our capacity to heal. This design-led research aims to reimagine regenerative and biophilic design as therapeutic environments as living systems that nurture both people and planet. Working from the vision of healthcare spaces as participants in ecological restoration, it investigates how co-design processes can enable healthcare and community environments to foster biodiversity, resilience, and deeper human-nature connection.
This research aims to advance a systems approach and asks:
- How might we co-design therapeutic environments to enhance both human wellbeing and ecological vitality.
- What design principles might support people and spaces as living for healing and regeneration.
- How do multidisciplinary networks navigate tensions between user needs, regenerative aspirations and healthcare or policy requirements.
Closing date : 9 January 2026
(29) Funded PhD Opportunities
Summary/title: Carbon-Negative self-healing enzymatic construction materials
This PhD project targets the development and evaluation of a durable self-healing construction material as a practical alternative to conventional concrete. The core innovation is the use of carbonic anhydrase (CA), a naturally occurring, low-cost, and readily available enzyme, to catalyze rapid CaCO₃ precipitation that plugs pores and repairs cracks in the paste matrix faster than current approaches. By accelerating sealing at early stages of damage, the material aims to prolong service life across both cement-based and non-traditional binders. Because CA consumes ambient CO₂ during catalysis, the approach also offers a route to co-benefits in the environment, notably mitigating algal overgrowth in marine systems, a growing challenge that threatens coral ecosystems, disrupts water treatment/quality, and increase microbial induced corrosion.
Closing date : 9 January 2026
(30) Funded PhD Opportunities
Summary/title: Beyond net-zero housing – community-driven decision tools for energy retrofit based on carbon-sequestering materials
Energy retrofits of existing buildings play a critical role in reducing energy demand and cutting carbon emissions. This project aims to evaluate carbon-sequestering materials, such as hempcrete and biochar composites, which have the potential to store carbon and provide thermal insulation and structural improvement. The project will assess their technical performance, identify barriers to adoption and explore cost-effective solutions. A decision-making tool will be developed to help homeowners, housing associations and policymakers identify the most suitable materials and methods based on performance, cost and climate.
Closing date : 9 January 2026
(31) Funded PhD Opportunities
Summary/title: AI for regenerative finance: sustainable, inclusive, and transparent capital flows
This project investigates how Artificial Intelligence (AI) can be designed and deployed to advance regenerative finance, a financial system that restores environmental health, fosters social inclusion, and supports long-term sustainability. The study aims to:
- Develop trustworthy and transparent AI models for sustainable financial decision-making.
- Examine equity and inclusion by identifying and mitigating biases in algorithmic access to sustainable capital.
- Evaluate the environmental footprint of financial AI, exploring how computational choices influence sustainability outcomes.
Closing date : 9 January 2026
About The University of Dundee, Scotland, United Kingdom – Official Website
The University of Dundee[a] is a public research university based in Dundee, Scotland. It was founded as a university college in 1881 with a donation from the prominent Baxter family of textile manufacturers. The institution was, for most of its early existence, a constituent college of the University of St Andrews alongside United College and St Mary’s College located in the town of St Andrews itself. Following significant expansion, the University of Dundee gained independent university status by royal charter in 1967 while retaining elements of its ancient heritage and governance structure.
The main campus of the university is located in Dundee’s West End, which contains many of the university’s teaching and research facilities; the Duncan of Jordanstone College of Art and Design, Dundee Law School and the Dundee Dental Hospital and School. The university has additional facilities at Ninewells Hospital, containing its School of Medicine; Perth Royal Infirmary, which houses a clinical research centre; and in Kirkcaldy, Fife, containing part of its School of Health Sciences. The annual income of the institution for 2022–23 was £325.7 million of which £78.9 million was from research grants and contracts, with an expenditure of £330.2 million
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