Congratulations to Dr Raymond Staals, Postdoctoral Fellow in the Fineran Lab, who has been awarded a Fast-Start Grant of $300,000 in the 2015 Marsden Funding round. Raymond's project is entitled Restriction of gene transfer in pathogenic bacteria by a novel CRISPR-Cas system.
This year, more than $11.7M in new government funding has been awarded to University of Otago researchers to undertake 20 world-class research projects pushing the boundaries of knowledge in their fields.
CRISPR-Cas is a prokaryotic adaptive immune system that restricts horizontal transfer of foreign genetic elements which carry important genetic traits, such as antibiotic resistance and virulence. The three classical CRISPR-Cas systems have been studied extensively over the last few years, and this has led to a revolution in genome editing. Recently, bioinformatic analyses identified a fourth CRISPR-Cas system (Type IV) in several pathogenic bacteria. No experimental information is available about these systems. I will characterise the structural and enzymatic properties of Type IV CRISPR-Cas to address key fundamental questions about this system and its role in controlling horizontal gene transfer.
Professor Greg Cook is co-principal investigator of a project which will investigate anti-microbial resistance mechanisms in Staphylococcus aureus. The project, Game of clones: unravelling biocide resistance mechanisms in Staphylococcus aureus has been awarded a grant of $490,000 over 2 years and will be led by Dr Deborah Williamson of the Department of Pathology & Molecular Medicine, University of Otago, Wellington.
Chlorhexidine (CHX) is a topical antiseptic used extensively in the clinical setting. We recently discovered a high prevalence of CHX resistance in New Zealand S. aureus isolates, with high rates of co-resistance to another common antibiotic, fusidic acid. In this project, we will determine: (i) the evolution and transmissibility of CHX resistance in S. aureus; (ii) why some strains of S. aureus take up CHX resistance genes, and (iii) whether the presence of these genes confers any bacterial fitness cost. Such knowledge may identify novel strategies and therapeutic targets that limit the emergence and spread of resistant S. aureus.