Are you holding Master’s degree and looking for fully funded PhD positions? University of Dundee, Dundee, Scotland invites online application for multiple funded PhD Programs / fully funded PhD positions in various research areas.
Candidates interested in fully funded PhD positions can check the details and may apply as soon as possible. Interested and eligible applicants may submit their online application for PhD programs via the University’s Online Application Portal.
1. Fully Funded PhD Position in AI-Driven Biomarker Discovery and Validation in Parkinson’s Disease through the MJFF LITE Initiative
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
2. Fully Funded PhD Position in Decoding a New Signalling Axis in Parkinson’s Disease
Summary of PhD Program:
Mutations in the kinase LRRK2 are one of the most common inherited causes of Parkinson’s disease, yet we still don’t fully understand how LRRK2 drives disease at the molecular level (1, 2). Our lab aims to change that, by uncovering how LRRK2 signalling is regulated, how it malfunctions in Parkinson’s disease, and how these insights can guide the discovery of new biomarkers and therapeutic targets.
Application Deadline: 31 October 2025
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3. Fully Funded PhD Position in A new biological mechanism for protein regulation
Summary of PhD Program:
One of the key challenges in molecular biology is to understand how post-translational modification events regulate protein function. In the Maniaci lab, we aim to uncover how proteases generate new protein fragments and how these fragments contribute to cellular homeostasis and disease development. Proteolysis is an irreversible post-translational modification that not only regulates protein stability but also creates fragments with distinct activities, interactions, and localisation1.
Application Deadline: 31 October 2025
4. Fully Funded PhD Position in Crosstalk between UPR Signaling and ER-phagy during ER Stress
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
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5. Fully Funded PhD Position in New technologies to monitor assembly of alternative forms of the proteasome
Summary of PhD Program:
The Rousseau lab is dedicated to decoding how proteasome-mediated protein degradation is regulated in cells to prevent the harmful accumulation of unfolded, misfolded, or damaged proteins. The proteasome recognises, unfolds, and degrades proteins tagged with ubiquitin, thereby safeguarding proteome integrity. By degrading 80–90% of intracellular proteins, the proteasome is a central hub of the protein homeostasis network, preventing the toxic buildup of protein aggregates that can impair cellular function.
Application Deadline: 31 October 2025
6. Fully Funded PhD Position in Viral interference of ISG15 signals
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
7. Fully Funded PhD Position in Genome Bodyguards: Investigating the Cell’s Hidden Repair Team
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
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8. Fully Funded PhD Position in How do Dysregulated Signalling Pathways cause Intellectual Disability?
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
9. Fully Funded PhD Position in Destroying cancer-causing proteins
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
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10. Fully Funded PhD Position in Discovery of novel organelle and ubiquitin mechanisms underlying Parkinson’s disease
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
11. Fully Funded PhD Position in Deciphering novel ALS signalling pathways: Biomarker discovery and developing therapeutic strategies
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
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12. Fully Funded PhD Position in Unravelling the molecular mechanisms of amyotrophic lateral sclerosis/motor neuron disease
Summary of PhD Program:
Our lab studies two ALS mutations—C9ORF72 (which also causes fronto-temporal dementia) and NEK1—using state-of-the-art human induced pluripotent stem cell models combined with CRISPR/Cas9 genome editing to generate motor neurons and also microglia. We are particularly interested in dissecting out the proximal cellular signalling pathways involved in pathogenesis and we use quantitative ultrasensitive proteomics and phosphoproteomics (including of key neuronal compartments, such as the axon) to help address this, with mechanistic studies performed initially in mammalian cell lines.
Application Deadline: 31 October 2025
13. Fully Funded PhD Position in Structural and Chemical Biology of Ubiquitin E3 Ligases
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
14. Fully Funded PhD Position in Investigating the immune-epithelial interactions that drive intestinal inflammation
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
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15. Fully Funded PhD Position in Decoding the hidden language of ubiquitin: non-canonical ubiquitylation in human health and disease
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
16. Fully Funded PhD Position in Decoding the mechanism and function of ER-Ribosome associated Quality Control
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
17. Fully Funded PhD Position in Finding the eat-me signals
Summary of PhD Program:
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.
Application Deadline: 31 October 2025
18. Fully Funded PhD Position in Defining the cellular fingerprint of motor neuron disease
Summary of PhD Program:
This PhD project will be carried out in the laboratory of Dr. Leeanne McGurk at the University of Dundee. The McGurk lab has made fundamental discoveries into TDP-43 biology and identified novel disease-modifying pathways, including the role of PARPs, stress response mechanisms, and RNA-binding proteins in controlling TDP-43 localisation and toxicity.