Education

​​

• 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. 

Education

• 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.

Education

• 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.

Education

​

• 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. 

Education:

• 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.