Campbell Gourlay began his career at The John Innes Centre in 1996 where he studied the genetic control of leaf development. Following this he began to work with budding yeast as a model eukaryote in the lab of Kathryn Ayscough, where he investigated the role of actin in the process of endocytosis. During this time he discovered a link between actin, the regulation of mitochondrial function and the control of ageing and apoptosis. This led to his involvement in the emerging field of yeast apoptosis, which has popularised the novel concept that unicellular organisms possess the ability to undergo programmed cell death as an altruistic act for the betterment of a population. In 2006 he was awarded a five year MRC Career Development Fellowship to establish his own lab within the Kent Fungal Group at the University of Kent where is now a senior lecturer in cell biology. The Gourlay lab maintains a strong interest in the role that actin plays in the control of homeostatic mechanisms that contribute to healthy ageing. The lab also uses yeast as a model eukaryote to study a number of aspects of human disease. The group has also diversified to apply its understanding of yeast stress signalling processes and death to the fields of fungal pathogenesis and drug resistance. 



Visit Campbell​​'s page on the University of Kent website​​​​​​​​​​​


Dr. Campbell Gourlay

Patrick Rockenfeller - Research Fellow


  • 2001-2006, University of Tübingen, Germany, Diplom Biochemistry (equivalent to MSc)

  • 2004-2005, University of the Mediterranean Aix-Marseille II, France, Erasmus stay funded by a Baden-Württemberg Fellowship

  • 2007-2010, University of Graz, Austria, PhD in Biochemistry and Molecular Biology

  • 2010-2015, University of Graz, Austria, Post doctoral Research Associate

  • 2015-present, University of Kent, UK, Post-Doctoral Research Fellow funded by the Austrian Science Fund (Erwin Schroedinger Fellowship)


Research Project


I am interested in lipid biology and its implication in cellular processes like autophagy, cell death, cytoskeletal regulation, MAPKinase signalling and mitochondria. Saccharomyces cerevisiae is the predominant model organism used in my studies.


My current project in the KFG within the framework of the Erwin Schroedinger fellowship aims at elucidating the interaction of mitochondria and Cofilin. Cofilin is a member of the ADF/Cofilin family of small actin binding proteins found in all eukaryotic cells, which are essential for dynamic polymerisation and depolymerisation of the actin cytoskeleton. However, despite their importance to the function of all eukaryotic cells, Cofilin proteins remain greatly underappreciated and under-researched. Subtle changes to the charged surfaces of Cofilin have a profound effect on the activity and quality of mitochondrial function. Importantly, the regions of Cofilin that are involved in controlling mitochondrial function are distinct from the actin binding and regulatory surface. 

Lucian Duvenage - PhD student



  • 2012, University of Cape Town, MSc Molecular Biology

  • 2014, University of Aberdeen, MRes Medical Mycology and Fungal Immunology


Research Project


Candida albicans is the major fungal pathogen in humans. C. albicans has three electron transport chain pathways; in addition the classical pathway shared with vertebrates, there is also a parallel pathway and an alternative pathway. The alternative pathway consists solely of the terminal oxidase known as alternative oxidase, which is insensitive to cyanide inhibition. The alternative pathway is not coupled to ATP synthesis and its role in stress responses remains unclear. The cell wall of C. albicans is critical for morphogenesis and virulence of the fungus, and its composition influences recognition by the immune system.


Mitochondria have many functions besides ATP production, including the synthesis of important lipids and resistance to antifungals. It is not known how electron transport chain function influences the composition of the cell wall, morphogenesis and virulence. In my project I will seek to answer these questions, focusing on the role of the electron transport chain in response to cell wall stresses and antifungals, and the signalling pathways induced in response to mitochondrial damage. This will evaluate the mitochondrion as a potential antifungal drug target.

Elliot Piper-Brown - PhD student



  • 2011-2014, University of Kent, BSc (Hons) Biomedical Science

  • 2014-2015, MSc Cell Biology

  • 2015-present, PhD student


Research Project


Ras proteins are small GTPases that function as regulatory switches linking external environmental stimuli with intracellular effectors to control cell growth and proliferation. Mutations that lead to the constitutive activation of Ras proteins are associated with the development of several human cancers. The localisation of Ras is crucial for its function and this is controlled by post-translational modifications. The genes encoding Ras proteins are highly conserved and yeast serves as a useful model to study the control of localisation and activation. We have identified that the phosphorylation of Serine225 plays an important role in the localisation and function of Ras2p in S. cerevisiae. Modification of this residue leads to changes in Ras localisation and controls a switch that drives cells towards a senescence phenotype via a previously unidentified cAMP/PKA signalling pathway. The Serine225 motif appears to be present within the human oncogene N-Ras, which may be suggestive of a conserved regulatory role for this phosphorylation event.

Daniel Pentland - PhD student


  • 2012 – 2015, University of Kent, BSc (Hons) Biology

  • 2015 – present, University of Kent, PhD Cell Biology


Research Project

A total laryngectomy is a surgical procedure for people with advanced laryngeal cancer which involves the removal of the entire larynx (including the vocal cords). Total laryngectomy patients are unable to speak following the procedure and often have to use a voice prosthesis (a small silicone valve inserted in a hole between the trachea and oesophagus) to restore their speech.

As with any foreign object within the body, voice prostheses are a constant source of infection. In particular, they are susceptible to biofilms formation which, if left to grow, eventually blocks the valve and causes the voice prosthesis to fail. This is a persistent problem with the average voice prosthesis only lasting approximately 6 months before needing to be changed in an invasive procedure. One of the main microorganism species colonising these voice prostheses, and certainly the primary fungal pathogen, is Candida albicans.

The level of CO2 in exhaled breath is approximately 150x that in normal air (~5% compared to 0.03%), meaning voice prostheses are consistently bathed in CO2. It has been shown that CO2 plays a significant role in the promotion of the C. albicans biofilm growth on voice prostheses. As part of my project I am investigating C. albicans biofilm growth on a molecular level, combining this new knowledge with clinical expertise in a multidisciplinary team (MDT) to provide more effective treatment/maintenance options to increase the lifespan of voice prostheses. 

Viktorija Makarovaite - PhD student



  • 2006-2010, Lewis University, BSc (Hons) Biology (Biochemistry (minor)

  • 2010-2012, Rush University, MSc Medical Laboratory Science (previously known as Medical Technology)

  • 2014-2015, Manchester University, MSc (Distinction) Medical Mycology

  • 2015- Present, University of Kent, PhD


Research Project

We are trying to develop a Radio Frequency Identification (RFID) biosensor which will be able to sense Candida spp. biofilm growth on voice prostheses.  Ultimately, the goal is to make the RFID biosensor compatible with mobile devices, which has already been done to an extent (in a none-fungal or bacterial capacity) at the University of Kent. It would allow the patients to receive a mobile updates on the “health” of their voice prostheses and warn them (and their physicians) of biofilm growth once it occurs. This research can help change the face of medical treatments because of its overlapping capability with other medical devices such as incorporation in neonatal catheter lines. Also, we are trying to develop anti-fungal polymers to replace medical silicone or to be used as an extra coating in the prevention of fungal growth on medical devices. 

Ryan Norman - PhD student



  • 2008-2011, Canterbury Christ Church University, BSc (Hons) Biological Sciences

  • 2016-2017, University of Kent, MSc Infectious Diseases

  • 2017-present, University of Kent, PhD 


Research Project


Tracheotomy tubing is a vital medical device which provides free airflow to the lungs in patients who cannot breathe for themselves normally. When these tubes are within a patient, organisms can grow on them in a biofilm, potentially activating as a source of infection and sometimes necessitating the replacement of the device. Previous research has shown that in practice many of these biofilms are comprised of multiple organisms, most notably the fungus Candida albicans, and the bacteria species Pseudomonas aeruginosa and Staphylococcus aureus.

I am investigating tracheotomy tubing from local patients in an effort to work out exactly which species are present, and hopefully determine the order of colonisation for these organisms. This could potentially lead to useful strategies for preventing their growth. 


I will also be carrying on some work from other members of the lab, investigating if the Alternative Oxidase present in Candida plays a role in biofilm formation and the Pseudomonas - Candida interaction (as Pseudomonas can produce pyocynin which can inhibit AOX in Candida). There are other candidates for investigation with the relationship of mixed biofilms - for example, the potential role of Nitric Oxide (NO).

Kevin Doyle - PhD student


  • 2012, University of Kent, BSc Biology.

  • 2015, University of Kent, MRes Cell biology and Ageing

  • 2017-present, PhD student, University of Kent


Research Project


Amyotrophic Lateral Sclerosis (ALS) is a motor neuron disease characterised by progressive degeneration of motor neurons in the brain and spinal cord. Mutations in the gene SOD1 are associated with 20% of familial ALS (fALS) cases. Aggregation of mutated, unstable Sod1 is thought to give rise to fALS through a toxic gain-of function. Recently, it has been shown that it is not just the insoluble aggregates of mutant/misfolded Sod1, but actually soluble mutant Sod1 that are damaging a range of cellular processes. Despite significant research efforts, there is still no effective therapy for ALS, indicating that there is still a lot to learn.


In a recently developed Yeast model of ALS, it was shown that ALS-linked SOD1 mutations leads to metabolic dysfunction and promotes senescence in the cell. Mutant Sod1 protein was shown to prevent acidification of the vacuole. The yeast vacuole is akin to the mammalian lysosome in that it plays a role in autophagy, metal ion homeostasis, cytosolic pH and other key metabolic processes. My project will aim to investigate the mechanism in which mutant/ misfolded Sod1 proteins disrupt metabolic processes in yeast, worm and human cell models.

James Dowling - MRes Student


  • 2014-2017, University of Surrey, Bachelor of Science Biochemistry

  • 2017- present, MRes in Cell Biology, University of Kent


Research Project:


“Investigating the role of translation control in healthy ageing”


Processes related to ageing where the relationship between activity loss and ageing is thought to be causative include mitochondrial function, autophagy and proteasome functions, and DNA maintenance and repair. More recently, protein translation has been included in this list. It is known that translational fidelity is actively maintained during healthy ageing in the face of many cellular alterations that would otherwise work to its detriment. In my project I will study the place fidelity control has in the multi-factorial process of cellular ageing.

Jack Davis - MRes Student


  • 2013-2016- University of Kent, BSc Biochemistry

  • 2017- University of Kent, MRes Cell Biology


Research Project


Lipid droplets are organelles within cells with a wide variety of processes, including conversion of free fatty acids to safer, neutral lipids for storage, and acting as buffers during times of oxidative stress.  


My project is to explore the link between mitochondria and lipid droplets, and more broadly, the roles that they each play with regards to cellular aging.  Using saccharomyces cerevisiae as a model, we aim to observe lipid droplet interactions with other cellular components during times of stress, such as heat shock and exposure to high levels of ROS.

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