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 Improving the Reliability and Economy of Anchors for Floating Offshore Wind Energy
Summary of PhD Program:
This research aims to optimize the effectiveness of site investigation for the geotechnical design of FOWT anchors, resulting in a significant reduction in cost. This will be done by developing a reliability-based risk assessment framework. The uncertainties arising from the site characterisation process and anchor capacity prediction models will be evaluated, respectively. Building on these, a comprehensive reliability-based risk analysis model will be developed for FOWT anchors.
Application Deadline: 31 October 2024
2. Fully Funded PhD Position in How do bacteria adapt survive in the lungs of patients with chronic lung infections like bronchiectasis?
Summary of PhD Program:
In this project we will investigate the molecular mechanisms by which H. influenzae or P. aeruginosa adapt and survive in the lungs of patients with bronchiectasis. The project will involve culturing clinical isolates and lab strains in vitro in the presence of other bacteria and immune products in a range of microbiological assays to understand variation between bacterial responses, both functionally and at the transcriptional level. Whole genome sequencing will then be used to see genetic difference between strains and detect contributing virulence factors. Any potential virulence factors will then be validated in laboratory strains.
Application Deadline: 31 October 2024
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3. Fully Funded PhD Position in Impact of the alarmin Il-33 on neutrophilic inflammation in chronic lung disease
Summary of PhD Program:
In this project we will investigate the in-vitro and in-vivo impact of IL-33 blockade on neutrophilic inflammation. The project will involve culture of primary neutrophils and epithelial cells from people with chronic lung disease and healthy controls, cell stimulation with IL-33 followed by targeted assays and proteomics, and analysis of biological samples obtained from clinical trials in which patients are receiving anti-IL33 monoclonal antibodies. In addition to tissue culture, key laboratory techniques will include primary cell isolation, flow cytometry, immunohistochemistry and fluorescence microscopy, ELISA and functional assays.
Application Deadline: 1 November 2024
4. Fully Funded PhD Position in Beyond Lysine: Exploring the Functional Consequences of Non-Canonical Ubiquitination in Health and Disease
Summary of PhD Program:
The De Cesare Lab’s mission is to understand the functional landscape of non-canonical ubiquitination and its impact on health and disease. Our lab has pioneered the identification of several non-canonical ubiquitin conjugating enzymes (E2s) – UBE2Q1, UBE2Q2, and UBE2QL1 – that mediate ubiquitin attachment to non-lysine residues [1]. Notably, UBE2Q1 knockout mice exhibit infertility due to defective embryo implantation, highlighting the critical role of these non-canonical E2s in early developmental processes and reproductive biology [2]. Additionally, altered expression of UBE2Qs has been observed in various human cancers, raising important questions about their roles in human health and disease.
Application Deadline: 31 October 2024
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5. Fully Funded PhD Position in Discovery of novel mitochondrial and organelle 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 2024
6. Fully Funded PhD Position in How do atypical E3 ligases facilitate their biology?
Summary of PhD Program:
Our multidisciplinary lab has developed pioneering technologies for E3 ligase discovery and activity measurement 1,2. The discovery and study of atypical E3 ligases have resulted in new ubiquitin system paradigms with therapeutic opportunities 3-5. We revealed that MYCBP2 conjugates ubiquitin to atypical sites such as threonine and uses an unprecedented ubiquitin transfer mechanism we term ubiquitin relay. MYCBP2 promotes programmed axon degeneration so drugs that block its ability to carry out non-lysine ubiquitination have great promise for treating neurological diseases such as multiple sclerosis, neuropathies and ALS.
Application Deadline: 31 October 2024
7. 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 2024
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8. Fully Funded PhD Position in Cleave to Modify: A new biological mechanism for protein regulation
Summary of PhD Program:
This project aims to identify novel substrateis and pathways regulated by the “cleave-to-modify” mechanism and link these discoveries to a cellular function. What makes this project especially exciting is its potential to reveal unprecedented fundamental pathway responsible for regulation of homeostasis, the disruption of which causes disease. By uncovering the role and extent of this unprecedented mechanism, the proposed project will transform our understanding of protein processing and modification and, consequently, reveal new potential targets for pharmacological intervention.
Application Deadline: 31 October 2024
9. Fully Funded PhD Position in Decoding the mechanism and function of UFMylation in ER 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 2024
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10. Fully Funded PhD Position in Understanding the physiological roles and pathological impacts of ER-Autophagy
Summary of PhD Program:
Autophagy is a lysosomal degradation pathway that is activated upon stress to facilitate clearance of damaged/toxic intracellular contents and recycle essential building blocks to sustain cell survival. The Liang Lab has a particular interest in understanding the physiological roles and pathological impacts of endoplasmic reticulum-specific autophagy (ER-phagy). We previously performed genome-wide CRISPR/Cas9 screens and uncovered many novel players that regulate ER-phagy (Liang and Corn, 2022). This includes a Ubiquitin-like modification, known as UFMylation, which we implicated in ER-phagy and ER stress regulation (Liang et al., 2020, Liang et al. 2018).
Application Deadline: 31 October 2024
11. Fully Funded PhD Position in Identifying therapeutically-targetable mechanisms of PIK3CA mutant-specific signal transfer
Summary of PhD Program:
The Madsen Lab is dedicated to a systems understanding of PI3K signalling plasticity, inspired by observations from human disorders such as cancer and PIK3CA-related overgrowth spectrum (PROS) 1,2. Over the last five years, with support from Wellcome funding, we uncovered previously unappreciated allele dose-dependent effects of PIK3CA mutations in human pluripotent stem cells and cancer 3–5. Recently, we also developed a versatile single-cell experimental framework for studies of quantitative, PI3K-dependent information transfer, demonstrating for the first time that the most frequent oncogenic PIK3CA mutation, PIK3CAH1047R, is not a simple ON switch of the pathway as commonly assumed. Instead, PIK3CAH1047R corrupts the ability of cells to resolve the identity of different growth factors, akin to “blurred” signal transfer.
Application Deadline: 31 October 2024
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12. Fully Funded PhD Position in Molecular mechanisms underlying Parkinson’s disease
Summary of PhD Program:
There is great need for improved understanding of the mechanistic biology underlying Parkinson’s disease. Such knowledge will help with development of new drugs that slow or even halt the progression of the disease. The discovery that hyper-activating mutations in a protein kinase termed LRRK2 causes Parkinson’s, offers the prospect of elaborating new, potentially disease-modifying treatments 1-3. Recent advances point towards LRRK2 controlling autophagy and lysosome function by phosphorylating a group of Rab GTPase proteins and regulating their ability to bind cognate effector proteins 1.
Application Deadline: 31 October 2024
13. Fully Funded PhD Position in How do Dysregulated Signalling Pathways cause Intellectual Disability?
Summary of PhD Program:
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).
Application Deadline: 31 October 2024
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 signalling components in 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 IEL to function. In this project, the student will learn to use state-of-the-art techniques including proteomics and phosphoproteomics, signalling studies to investigate the pathways regulating IEL responses, Ribo-Seq to rapidly identify changes in IEL, and in vivo models to address how perturbations in signalling pathways regulate intestinal homeostasis.
Application Deadline: 31 October 2024
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15. Fully Funded PhD Position in The antiviral roles of ISG15 modifications
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 a unique opportunity to work at the bench alongside their supervisor and the opportunity to participate in several internal and external collaborations.
Application Deadline: 31 October 2024
16. Fully Funded PhD Position in New technologies to monitor assembly of alternative forms of the proteasome
Summary of PhD Program:
The PhD project aims at engineering the proteasome to develop new technologies to monitor assembly of its alternative forms suitable for high-throughput screening. This will be instrumental in better understanding the function of alternative forms of the proteasomes and will help understand their involvement in diseases. 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).
Application Deadline: 31 October 2024
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. 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.
Application Deadline: 31 October 2024
18. Fully Funded PhD Position in Destroying cancer-causing proteins
Summary of PhD Program:
This PhD project aims to understand the molecular mechanisms by which FAM83F and FAM83G activate Wnt signalling and explore if targeted degradation of FAM83F and/or FAM83G inhibits Wnt-dependent proliferation of colorectal and other cancers. 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 FAM83F/FAM83G, and development and application of small molecule degraders, including PROTACs and molecular glues, of FAM83F-CK1-alpha and FAM83G-CK1-alpha complexes.
Application Deadline: 31 October 2024
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19. Fully Funded PhD Position in Location, location, location: DNA damage sensors which launch protective responses to DNA damage
Summary of PhD Program:
DNA damage happens at very high frequency in the cells in our bodies – meaning that the instructions for the proper functioning of cells could be altered unless the mistakes are spotted and corrected. We recently started a search for new surveillance factors in human cells that can detect damaged DNA and help to launch the DDR “DNA damage response” that stops secondary consequences of DNA damage such as mutations, disease or cell death (see for example EMBO Journal 40, e108271).
Application Deadline: 31 October 2024
20. Fully Funded PhD Position in Translational Studies into Molecular mechanisms underlying Parkinson’s disease
Summary of PhD Program:
This project will be embedded in the newly funded ‘The Michael J Fox Foundation LRRK2 Therapeutic Exchange Initiative’ (MJFF-LITE) and in close collaboration and co-supervision by Professor Dario Alessi (second PhD supervisor). Clinically, PD is highly heterogenous but there is a ‘LRRK2 driven’ subtype that needs to be better defined as these patients will most likely benefit from LRRK2 targeting treatment strategies. Pathogenic variants (mutations) in LRRK2 hyperactive the LRRK2 kinase with subsequent RabGTPase hyperactivation leading to dysregulated endolysosomal trafficking and lysosomal dysfunction (1).
Application Deadline: 31 October 2024
21. Fully Funded PhD Position in Pharmacogenetic and proteomic characterisation of response to Dipeptidyl peptidase-1 inhibitors: precision medicine for a novel class of anti-inflammatory drugs
Summary of PhD Program:
This project will combine a clinical translational study, investigating the proteome and transcriptome of neutrophils from different patient populations, and analysis of unique datasets (large population genetic datasets) and data taken from clinical trials of DPP1 inhibitors to investigate differences between patient groups in the neutrophil proteome, neutrophil functional responses, the genetics of DPP1 and its target proteases and how this translates into different responses to DPP1 inhibitors. Full training will be provided in bioinformatic and wet lab techniques.
