Bacteria or virus spheres

Our Cell Engineering research covers topics such as protein folding in the secretory pathway, regulation of membrane traffic, control of cell cycle, cytokinesis, compartmentalization of cellular signalling and cell engineering.

PhD Research Projects

Self funded opportunities

Defining the mechanism of abscission

Outline & aim

ESCRT proteins mediate membrane scission events involved in the down-regulation of ubiquitin-labelled receptors via the multivesicular body (MVB) pathway and in HIV budding from host cells. In addition, ESCRT proteins play a role in abscission, the final stage of cytokinesis. The ESCRT machinery is composed of four complexes: ESCRT-0, -I, -II and -III; and the modular composition of the ESCRT machinery is reflected in its various functions. At a precise time during cytokinesis, the ESCRT-I protein TSG101 and ESCRT-associated protein ALIX are recruited to the midbody through interactions with CEP55; TSG101 and ALIX in turn recruit ESCRT-III components. Thereafter, by a mechanism still not completely understood, ESCRT-III redistributes to the putative abscission sites, microtubules are severed and the daughter cells separate. However, the mechanisms by which this selective and specific redistribution of ESCRT proteins is regulated in space and time remain largely unsolved.

ESCRT components are phosphoproteins, so we reasoned that kinases and phosphatases are likely candidates for ESCRT regulation. We hypothesised that polo and aurora kinases and Cdc14 phosphatase may be potential regulators of ESCRT function due to their significant roles in controlling cytokinesis. This aspect of mitotic regulation of

ESCRT function will be investigated in this project, as we have shown that these kinases and phosphatases play a role; our challenge now is to define that role and to determine whether similar mechanisms operate in mammalian cells. This interface between signalling and trafficking is an important and active research theme worldwide, and you will join an active and collaborative group well versed in all the training aspects required for successful completion of a PhD.

The aim of the project is to define the role of aurora kinase, polo-like kinase and Cdc14 on ESCRT function in yeast and mammalian cells.

Techniques

Yeast genetics; molecular biology; mammalian cell culture and cell biology; high resolution imaging/confocal microscopy

References

  • M.S.Bhutta, B.Roy, G.W.Gould and C.J.McInerny Public Library of Science 1. (2014) In press. “Control of cytokinesis by polo and aurora kinases and Cdc14 phosphatase regulation of ESCRT proteins.”
  • H.Neto, A.Kaupisch, L.L.Collins and G.W.Gould. Molecular Biology of the Cell (2013) 24, 3633-3674. “Syntaxin 16 is required for early stages in cytokinesis.”

Contact

gwyn.gould@glasgow.ac.ukchris.mcinerny@glasgow.ac.uk

Developing novel, combined strategies for peripheral nerve repair

Outline & aim

Peripheral nerve injuries are frequently seen following trauma or malignancy, with an incidence of 300000 cases in Europe following trauma alone. These injuries often result in functional deficits, and have a high impact on the patient’s quality of life, as well as placing a heavy financial burden on the state. Despite advances in surgical treatments, motor and sensory recovery following these injuries often remains incomplete. Here we help develop materials and apply a variety of biophysical techniques ranging from ultrasonic manipulation to 3D micro fabrication and microfluidics to create artificial guidance tubes, or tissues, that aid in nerve repair, with the aim of improving and assisting the outcome of surgical nerve repair.

The materials and devices are tested in vitro using a variety of models for peripheral and central nerve repair. The projects available range from basic materials science in collaboration with chemists (Prof G Cooke, Dr R Hartley, Prof M Salmeron-Sanchez), engineers for active nerve stimulation (Prof D Cumming) acoustic placement (Prof Cummings & Dr A Bernassau), microfluidics (Dr H Yin), to applied models (Prof A Hart). The implications of the different repair strategies on the cells genomic and proteomic response is being investigated in collaboration with the Glasgow Polyomics Facility (Dr R Burchmore, P Herzyk). This work is very much interdisciplinary, and adventurous, and requires not only a good foundation in basic molecular and cell biology, but also a willingness to learn the language and science of chemists, materials scientists, engineers and surgeons.

The project will vary depending on the applicants abilities and specific interests, the techniques and supervisors mentioned below are those with whom Dr Riehle collaborates.

Techniques

Primary cell culture, molecular biology, imaging, image analysis, then depending on the specific project collaboration with engineers, chemists or physicists to make materials - synthetic organic chemistry - micro fabrication - electronic engineering - acoustic engineering.

References

  • Cortese, B., Gigli, G., & Riehle, M. (2009). Mechanical Gradient Cues for Guided Cell Motility and Control of Cell Behavior on Uniform Substrates. Advanced Functional Materials, 19(18), 2961–2968
  • Donoghue, P. S., Sun, T., Gadegaard, N., Riehle, M. O., & Barnett, S. C. (2013). Development of a Novel 3D Culture System for Screening Features of a Complex Implantable Device for CNS Repair. Molecular Pharmaceutics. doi:10.1021/mp400526n
  • Caldwell, S. T., Maclean, C., Riehle, M., Cooper, A., Nutley, M., Rabani, G., … Cooke, G. (2014). Protein-mediated dethreading of a biotin-functionalised pseudorotaxane. Organic & Biomolecular Chemistry, 12(3), 511–6. doi:10.1039/c3ob41612g
  • Gesellchen, F., Bernassau, a L., Déjardin, T., Cumming, D. R. S., & Riehle, M. O. (2014). Cell patterning with a heptagon acoustic tweezer - application in neurite guidance. Lab on a Chip, 19, 2266–2275. doi:10.1039/c4lc00436a
  • Martin, C., Dejardin, T., Hart, A., Riehle, M. O., & Cumming, D. R. S. (2013). Directed Nerve Regeneration Enabled by Wirelessly Powered Electrodes Printed on a Biodegradable Polymer. Advanced Healthcare Materials, 1–6. doi:10.1002/adhm.201300481
  • Nikukar, H., Reid, S., Tsimbouri, P. M., Riehle, M. O., Curtis, A. S. G., & Dalby, M. J. (2013). Osteogenesis of mesenchymal stem cells by nanoscale mechanotransduction. ACS Nano, 7(3), 2758–67. doi:10.1021/nn400202j

Contact

Mathis.Riehle@glasgow.ac.uk

Molecular Control of Mesenchymal Stem Cell Differentiation to Fat and Bone by Anti-Diabetic Drugs

Outline & aims

Bone health is impaired in both type 1 and type 2 diabetes mellitus (T1DM and T2DM) and an improved understanding of impaired bone health is a major unmet need in the field of diabetes mellitus (DM). Bone health is compromised during DM due to a shift in the balance of differentiation of mesenchymal stem cells (MSCs) from bone formation towards fat. We therefore aim to determine the molecular and cellular control of MSC differentiation to either fat (adipogenesis) or bone (osteogenesis) in the context of anti-diabetic drug treatment. This is important because the widely-used drug, metformin, has been reported to have anabolic effects on bone whereas other insulin-sensitising drugs, such as the thiazolidinediones (TZDs), reduce bone mineral density with a corresponding increase in marrow fat and fracture incidence [1,2]. This differential effect of commonly encountered anti-diabetic drugs on osteogenesis and adipogenesis needs further study as it may lead to a more effective approach to the combined management of bone health and glucose homeostasis in people with DM.

As many anti-diabetic drugs have been reported to influence AMP-activated protein kinase (AMPK) activity, which has been reported to alter bone formation [3], our working hypothesis is that AMPK signalling pathway plays a cardinal role in regulating these processes through the regulation of expression of Runx2 and PPAR? transcription factors. We will therefore determine the role of AMPK in the control of murine (pluripotent CH310T1/2 cells [4]) and human models (human bone marrow-derived MSCs) of MSC differentiation in response to osteogenic (metformin) and adipogenic (TZD) anti-diabetic drug treatment.

Techniques

Stem cell culture; light microscopy; confocal microscopy; immunofluorescence; reporter genes; western blotting

References

  • Muruganandan, S., Roman, A.A. and Sinal, C.J. (2009). Adipocyte differentiation of bone marrow-derived mesenchymal stem cells: cross talk with the osteoblastogenic program. Cell Mol Life Sci 66, 236-53.
  • Betteridge, D.J. (2011). Thiazolidinediones and fracture risk in patients with Type 2 diabetes. Diabet Med 28, 759-71.
  • Shah, M., Kola, B., Bataveljic, A., Arnett, T.R., Viollet, B., Saxon, L., Korbonits, M. and Chenu, C. (2010). AMP-activated protein kinase (AMPK) activation regulates in vitro bone formation and bone mass. Bone 47, 309-19.
  • Reznikoff, C.A., Brankow, D.W. and Heidelberger, C. (1973). Establishment and characterization of a cloned line of C3H mouse embryo cells sensitive to postconfluence inhibition of division. Cancer Res 33, 3231-8.

Contact

Stephen.Yarwood@glasgow.ac.uk

Molecular mechanics of clustering and gating in plant ion channels

Outline & aim

The organisation of ion channels in eukaryotic membranes is intimately connected with their activity, but the mechanics of the connections are, in general, poorly understood. Both in animals and plant, many ion channels assemble in discrete clusters that localise within the surface of the cell membrane. The clustering of the GORK channel — responsible for potassium efflux for stomatal regulation in the model plant Arabidopsis — is intimately connected with its gating by extracellular K+. Recent work from this laboratory yielded new insights into the processes linking K+ binding within the GORK channel pore to clustering of the channel proteins.

This project will explore the physical structure of GORK that determines its self-interaction as a function of the K+ concentration with the aim of understanding its integration with the well-known mechanics of channel gating.

Techniques

The student will gain expertise in molecular biological methods, and a deep grounding in the concepts of membrane transport, cell biology and physiology. Skills training will include in-depth engagement in molecular biology, protein biochemistry and molecular genetic/protein design, single-cell imaging and fluorescence microscopy, and single-cell recording techniques of electrophysiology using heterologous expression in mammalian cell systems and in plants.

References

  • Lefoulon, et al. (2014) Plant Physiol 166, 950-75
  • Eisenach, et al. (2012) Plant J 69, 241-51
  • Dreyer & Blatt (2009) Trends Plant Sci 14, 383-90

 Contact:

Michael.Blatt@glasgow.ac.uk

Photoregulation of plant hormone trafficking and signalling

Outline & aim

The phytohormone auxin (indole acetic acid) is instrumental for directing and shaping plant growth and form. Understanding how this chemical growth regulator controls plant development will have important implications for manipulating plant growth for agronomic gain. Auxin trafficking is profoundly influenced by many abiotic factors, including light. For instance, phototropin receptor kinases (phot1 and phot2) function to redirect auxin fluxes that are required to reorientate plant growth toward or away from light. The phot1-interacting protein Non-Phototropic Hypocotyl 3 (NPH3) is essential for establishing these light-driven auxin movements. However, the mode of action of NPH3 and how it functions to regulate transporter activity remains poorly understood.

This project aims to spatially dissect the site(s) of NPH3 action and how it impacts the subcellular trafficking and function of known auxin transporter proteins implicated in phototropism. Work is also focussed on characterising a newly identified NPH3 protein (NPH3-like, NPH3L) that interacts directly with phot1. Functional characterisation of NPH3, NPH3L and its homologues will provide new insights into the photoregulation of auxin trafficking and signalling associated with phototropism and other phototropin-mediated responses.

Techniques

This proposal is focused on characterising the molecular processes that integrate light and phytohormone signalling, two important agronomic processes associated with manipulating plant growth and optimising photosynthetic efficiency. Both these research areas fall squarely within the strategic priorities of Food Security, Living with Environmental Change and Crop Science. The project will provide excellent training in a range of techniques associated with molecular biology, cell biology, genetics and biochemistry. Training will also be given in key skills including teaching, project-management and science communication. Additionally, the student will have the opportunity to attend and present their research at the international photobiology meetings e.g. Gordon Research Conference in Photosensory Receptors and Signal Transduction, Galveston, Texas in 2016 (which I will chair).

References

  • CHRISTIE, J.M. (2007) Phototropin blue-light receptors. Annu. Rev. Plant Biol. 58, 21-45.
  • Sullivan, S., Thomson, C.E., Kaiserli, E. and Christie J.M. (2009) Interaction specificity of Arabidopsis 14-3-3 proteins and phototropin receptor kinases. FEBS Lett. 583, 2187-2193.
  • Christie, J.M., Richter, G., Yang, H., Sullivan, S., Thomson, C.E., Lin, J., Tiapiwatanakun, B., Ennis, M. Kaiserli, E., Lee, O.R., Adamec, J., Peer, W.A. and Murphy, A.S. (2011) Phot1 inhibition of ABCB19 primes lateral auxin fluxes in the shoot apex required for phototropism. PLoS Biol., 9(6): e1001076.
  • CHRISTIE, J.M. and MURPHY, A.S. (2013) Shoot phototropism in higher plants: New light through old concepts. Am. J. Bot. 100, 35-46.

Contact

John.Christie@glasgow.ac.uk

Regulation of plant nuclear architecture by light

Outline & aim

Light is essential for plant growth, development and photoprotection. One of the primary sites where light regulates major cellular processes is the nucleus. We are interested in elucidating how light stimulates the accumulation of photoreceptors and signalling components in nuclear micro-domains to regulate gene expression, chromatin remodelling and DNA damage repair. The student will investigate how nuclear compartmentalisation correlates with changes in the expression of growth promoting genes in response to light.

Techniques

A series of approaches will be used depending on the interests and background of the applicant: Gene expression analysis (qRT-PCR, ChIP), molecular cloning, protein interactions studies (Y2H, co-immunoprecipitation), protein characterisation (heterologous expression and purification), cell biology (confocal microscopy), plant genetics and plant physiology.

Contact

Eirini.Kaiserli@glasgow.ac.uk

The role of EPAC1 in the control of cytokine signalling in vascular endothelial cells

Outline & aims

We and others [1-3] have found that the cyclic AMP-activated signalling protein EPAC1 (exchange protein activated by cyclic AMP 1) promotes protective functions in vascular endothelial cells (VECs), including promotion of endothelial barrier function and induction of protein suppressors of cytokine signalling (eg SOCS3), and therefore plays a vital role in maintaining the health of the vasculature.

It is now clear that interactions with cellular binding proteins determine both the intracellular location and enzyme activity of EPAC1. For example, the cytoskeleton-associated, MAP1a-LC2 protein [4], recruits EPAC1 to microtubules and enhances its activity, whereas the nuclear-localised SUMO ligase, RanBP2 [5,6], suppresses EPAC1 activity at the nuclear pore complex.

Our aim now is to fully understand these control mechanisms with the long term goal of devising new therapies based on modulating protein interactions with EPAC1. Central to this goal is the new observation that EPAC1 becomes SUMOylated within the regulatory cyclic nucleotide binding domain (CNBD). Since the CNBD is responsible for direct activation by cyclic AMP and is also responsible for cytoskeletal recruitment through MAP1a-LC2, then SUMOylation represents a powerful new control mechanism for controlling EPAC1 localisation and activity.The student will therefore determine:

  1. The effects of SUMOylation on EPAC1 activity, subcellular localisation and interaction with regulatory proteins
  2. Determine the role of EPAC1 SUMOylation on the regulation of cytokine signalling in vascular endothelial cells

Techniques

Cell culture; light microscopy; confocal microscopy; immunofluorescence; reporter genes; western blotting

References

  • Sands, W.A., Woolson, H.D., Milne, G.R., Rutherford, C. and Palmer, T.M. (2006). Exchange protein activated by cyclic AMP (Epac)-mediated induction of suppressor of cytokine signaling 3 (SOCS-3) in vascular endothelial cells. Mol Cell Biol 26, 6333-46.
  • Yarwood, S.J., Borland, G., Sands, W.A. and Palmer, T.M. (2008). Identification of CCAAT/enhancer-binding proteins as exchange protein activated by cAMP-activated transcription factors that mediate the induction of the SOCS-3 gene. J Biol Chem. 283, 6843-53.
  • Borland, G., Smith, B.O. and Yarwood, S.J. (2009). EPAC proteins transduce diverse cellular actions of cAMP. Br J Pharmacol 6, 6.
  • Gupta, M. and Yarwood, S.J. (2005). MAP1A light chain 2 interacts with exchange protein activated by cyclic AMP 1 (EPAC1) to enhance Rap1 GTPase activity and cell adhesion. J Biol Chem 280, 8109-16.
  • Gloerich, M., Vliem, M.J., Prummel, E., Meijer, L.A., Rensen, M.G., Rehmann, H. and Bos, J.L. (2011). The nucleoporin RanBP2 tethers the cAMP effector Epac1 and inhibits its catalytic activity. J Cell Biol 193, 1009-20.
  • Liu, C., Takahashi, M., Li, Y., Dillon, T.J., Kaech, S. and Stork, P.J. (2010). The interaction of Epac1 and Ran promotes Rap1 activation at the nuclear envelope. Mol 30, 3956-69.

Contact

Stephen.Yarwood@glasgow.ac.uk

Overview

Our Centre for the Cellular Microenvironment at Glasgow is a new entity (2018) arising from the merger of the Centre for Cell Engineering (CCE) and the Microenvironments for Medicine (MiMe). We are focused on fostering education and training in research to develop microenvironments to investigate and instruct cellular behaviour including, but not solely, stem cell differentiation.

Our research is centred on exploring how cells respond to their environment by changes in behaviour, differentiation, metabolism and various aspects of development. Our goal is to apply the knowledge gained from our research to address key issues affecting (stem) cell biology. The Centre for the Cellular Microenvironment at Glasgow adopts an inter-disciplinary approach across the Institute of Molecular, Cell and Systems Biology (MCSB) in the College of Medical, Veterinary and Biological Sciences and the Bioengineering Group in the School of Engineering, which is part of the College of Science and Engineering. Cell-environment interactions, cell signalling, stem cell biology, cell, and protein structure and function at interfaces, bioengineering of gene regulation by microenvironments, nanoparticle technologies, synthetic biology to guide cell adhesion, cell sorting and translational approaches to take finding to clinical application.

Study options

PhD programmes typically last 3-4 years with research topics being allied to ongoing research within the Centre for the Cellular Microenvironment. Some projects are related to basic science and other projects are more focused on translational aspects of our research; but all projects integrate with our existing research themes. A variety of multi-disciplinary research approaches are applied within these research programmes, including biomedical engineering, protein engineering, biochemistry, molecular biology, biophysics, polyomics (genomics, transcriptomics, proteomics, metabolomics), biomaterials, bioinformatics and synthetic biology, as well as cellular imaging of biological functions.

Specific areas of interest include:

  • Bioengineering the microenvironment
  • Engineering approaches to control gene expression
  • Bio-engineered interfaces
  • Biomaterials, scaffolds and 3D printing
  • Protein structure and function
  • Protein engineering and application
  • Cell sorting and characterisation
  • Stem cell maintenance and differentiation
  • Nanoparticles for theranostics

Specific areas of application are:

  • Bone repair
  • Nerve repair
  • Sourcing of rare cells
  • Blood Brain Barrier
  • Mesenchymal stem cell niche
  • Haematopoietic stem cell niche

See Glasgow Biomaterials Seminar for an idea about recent and current projects.

Our PhD programme provides excellent training in cutting edge technologies that will be applicable to career prospects in both academia and industry.  Many of our graduates become postdoctoral research associates (Canada, USA, Europe and UK) while others go on to take up positions within industry either locally (e.g. Collagen Solutions, BioGelX) or overseas (e.g. Medtronic). We have strong national and international connections with many academic and industrial collaborators. Funds are available through the College of Medical, Veterinary and Biological Sciences or the College of Science and Engineering (depending on primary alignment) to allow visits to international laboratories, or industry where part of your project can be carried out. This provides an excellent opportunity for networking and increasing your scientific knowledge and skill set

Entry requirements

Awarded or expected 1st class or high upper 2nd class BSc degree.

English Language requirements for applicants whose first language is not English.

Fees and funding

Fees

2019/20

  • £4,320 UK/EU (to be confirmed by UKRI)
  • £21,020 outside EU

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Additional fees for all students:

  • Re-submission by a research student £500
  • Submission for a higher degree by published work £1,250
  • Submission of thesis after deadline lapsed £320
  • Submission by staff in receipt of staff scholarship £730
  • Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period) £300

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

Alumni discount

A 10% discount is available to University of Glasgow alumni. This includes graduates and those who have completed a Junior Year Abroad, Exchange programme or International Summer School at the University of Glasgow. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.

2018/19 fees

  • £4,260 UK/EU
  • £20,150 outside EU

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Additional fees for all students:

  • Submission by a research student £480
  • Submission for a higher degree by published work £1,200
  • Submission of thesis after deadline lapsed £300
  • Submission by staff in receipt of staff scholarship £680
  • Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period) £270

Depending on the nature of the research project, some students will be expected to pay a bench fee to cover additional costs. The exact amount will be provided in the offer letter.

Funding

Support

Resources

We offer a wide range of cutting-edge research facilities, including core facilities in

  • fluorescence activated cell sorting analysis
  • cell imaging and biophysical techniques, including NMR.
  • protein characterization that consists of state of the art machinery for analysing protein structure and interactions
  • mass spectrometry
  • next generation sequencing

Our research spaces are state-of-the-art and span three buildings. Notably, The Centre for Cell Engineering is a collaboration between biologists, physical scientists, engineers and clinicians aiming to understand the cell / material interface and the micro / nano scale.  And then building improved and new medical devices. In addition to increasing understanding of fundamental cell biology to new nano and micro material,  the Centre aims to translate cutting-edge science to clinic. 

Through their research interests in drug development, biotechnology and clinical applications, many of our project supervisors have strong links with industry. We also have strong academic conections with many international collaborators in universities and research institutes. Funds are available through the collage of MVLS to allow visits to international laboratories where part of your project can be carried out. This provides an excellent opportunity for networking and increasing your scientific knowledge and skill set.

Graduate School

The College of Medical, Veterinary and Life Sciences Graduate School provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
 
Our over-arching aim is to provide a research training environment that includes:

  • provision of excellent facilities and cutting edge techniques
  • training in essential research and generic skills
  • excellence in supervision and mentoring
  • interactive discussion groups and seminars
  • an atmosphere that fosters critical cultural policy and research analysis
  • synergy between research groups and areas
  • extensive multidisciplinary and collaborative research
  • extensive external collaborations both within and beyond the UK 
  • a robust generic skills programme including opportunities in social and commercial training

How to apply

Step 1: identify potential supervisors

Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor who will act as the main source of academic support and research mentoring. You may want to identify a potential supervisor and contact them to discuss your research proposal before you apply. Please note, even if you have spoken to an academic staff member about your proposal you still need to submit an online application form.

You can find relevant academic staff members with our staff research interests search.


Step 2: check the entry requirements

Entry requirements for postgraduate research vary.

All Postgraduate Research applicants should normally possess one or more of the following:

  • First or Upper Second Class Honours Degree or equivalent qualification (2:1 in the case of UK Research Council supported students).
  • In some cases a Masters qualification or equivalent is required

Candidates whose first language is not English must show evidence of appropriate competence in English. You can find the specific requirements on our international students pages.

Please check the relevant entry in the A-Z list of subject pages to find out any specific entry requirements and application documents.


Step 3: search for funding and scholarships

Search for funding and scholarships

As a commitment to supporting students and rewarding excellence, the University of Glasgow offers a wide range of scholarships


Step 4: gather your documents

Before applying please make sure you gather the following supporting documentation:

  1. Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document
  2. Degree certificates (and an official translation, if needed): scanned copy in colour of the original document
  3. Two references on headed paper (academic and/or professional).
  4. Research proposal, CV, samples of written work as per requirements for each subject area. Please check the relevant entry in our A-Z of subjects for specific details.

Submitting References

To complete your application we will need two references (one must be academic the other can be academic or professional).

There are two options for you to submit references as part of your application.  You can upload a document as part of your application or you can enter in your referee’s contact details and we will contact them to request a reference.

Option 1 – Uploading as part of the application form

Your references should be on official headed paper. These should also be signed by the referee. You can then upload these via theOnline Application form with the rest your documents to complete the application process.

Please be aware that documents must not exceed 5MB in size and therefore you may have to upload your documents separately. The online system allow you to upload supporting documents only in PDF format. For a free PDF writer go to www.pdfforge.org.

Option 2 - Entering contact details as part of the application form

If you enter your referees contact details including email on the application form we will email them requesting they submit a reference once you have submitted the application form.  When the referee responds and sends a reference you will be sent an email to confirm the university has received this.

After submitting your application form

You must submit details of two references during your application form.  If you need to submit another reference after you have submitted your application form (for example one referee is now unable to provide you with a reference) you must do this through the Applicant Self Service uploading documents function. 

If after you have submitted your application you required to upload a new reference and your referees would prefer to provide confidential references direct to the University then we can also accept the reference by email, from the referee’s official university or business email account to rio-researchadmissions@glasgow.ac.uk. We will then add these to your application.

If after you have submitted your application you required to upload a new reference and your referees would prefer to provide confidential references direct to the University then we can also accept the reference by email, from the referee’s official university or business email account to rio-researchadmissions@glasgow.ac.uk. We will then add these to your application.


Step 5: apply online

Once you have all your supporting documentation you can apply through our Online Application System


I've applied. What next?

If you have any other trouble accessing Applicant Self-Service, please see Application Troubleshooting/FAQs.

If you are requested to upload further documents

Log into the Applicant Self Service and scroll down to the Admissions Section. The screenshot below indicates the section on the page, and the specific area you should go to, highlighted in red:

Applicant self service

Documents must be uploaded in .jpg, .jpeg or .pdf format and must not exceed 5MB in size.  There is a maximum 10MB upload size for all documents with the application.

Decisions

Once a decision has been made regarding your application the Research Admissions Office will contact you by email.

If you are made an unconditional offer

You can accept your offer through the Applicant-Self-Service by clicking on the ‘Accept/Decline link’ for your chosen programme under the ‘Admissions Section’ at the bottom of the Applicant Self Service screen.  You can access the Applicant Self Service by using the link, username and password you used to apply and selecting the “Self Service” button below your application.

Please make sure you accept your unconditional offer within 4 weeks of receiving your offer. If you are an international student your CAS will not be issued until you have accepted an unconditional offer.

If you are made a conditional offer

If you accept a conditional offer then the offer status on Applicant-Self-Service will change to ‘incomplete’ to indicate that the application is incomplete until such time as all the conditions are met.

Your offer letter will list all the conditions that apply to your offer and you can upload the required document(s) through Applicant Self Service. If you have met the conditions satisfactorily, you will automatically be sent an unconditional offer.

If your application is unsuccessful

If your application is unsuccessful then we will send you an email to inform you of this which will outline the reason why we have been unable to offer you a place on this particular programme. Please note that your application status will be updated to 'Cancelled' on Applicant Self Service if the offer is rejected.

Deferring your offer

If you want to defer your start date, please contact us directly at rio-researchadmissions@glasgow.ac.uk. We need authorisation from your supervisor before we confirm your request to defer. Once we have this we will contact you by email to confirm.

How to register

After you have accepted an unconditional offer you will receive an email nearer to the start of your studies to tell you how to register online using the University's MyCampus website, the University’s student information system. That email will provide you with your personal login details and the website address. Please ensure that your email address is kept up to date as all correspondence is sent via email. You can update your email address through the Applicant Self Service Portal under the Personal Information section.

For more information and a step by step guide can be found on our Registry site.


Contact us

International Students