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Photo of bacterial cells (Pseudomonas aeruginosa) taken by Scanning Electronic Microscopy (SEM) *Niki Murray and Xue-Xian Zhang
A graphical abstract from the research project showing the molecular interaction between the bacteria and its host.
This project uses modern tools in molecular biology to elucidate the mechanisms of bacterial colonisation on the surfaces of plants and human tissues.
Bacteria have strict food preferences in terms of the order in which they uptake and utilise substrates: the underlying mechanism being carbon catabolite repression (CCR). CCR has been well studied in E. coli where it is mediated by the catabolite-activating protein (CAP) charged with cAMP. However, this paradigm does not hold for many non-enteric bacteria such as Pseudomonas fluorescens SBW25. SBW25 is a plant growth-promoting bacterium isolated from sugar beet leaves grown in Oxford University farm. It belongs to the same genus of Psa, the causative agent of kiwifruit bacterial canker. We found that SBW25 has evolved a very complex CCR mechanism to ensure preferential utilization of nutrients that coexist in the environments. Such knowledge will help understand how bacteria are fed in planta, and develop new methods such as the use of toxic nutrient analogues to control plant infectious diseases.
Targeting the mechanism of host recognition to prevent bacterial infections
With the widespread increase of bacterial resistance to antibiotics, new strategies to prevent and treat healthcare-associated infcetion (HAI) are urgently required. This project funded by the Auckland Medical Research Foundation (AMRF) addresses a crucial gap in our current understanding of how bacteria cause disease – namely, how pathogenic bacteria recognise vulnerable hosts for successful colonization and immune evasion.
To date, our research has focused on Pseudomonas aeruginosa, an environmental pathogen that causes a wide range of healthcare-associated infections and pulmonary infections in people with chronic lung diseases, particularly cystic fibrosis. We are testing a new hypothesis that P. aeruginosa recognises urocanate, a histidine metabolite accumulated in tissues such as skin, and use it as a trigger for bacterial invasion. The data will form the basis for the development of new strategies to prevent bacterial infection through interrupting the urocanate-mediated host recognition.
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Last updated on Tuesday 16 August 2016
- Institute of Natural and Mathematical Sciences
I am a microbiologist currently working in the fields of bacterial molecular genetics, bacterial pathogenicity, experimental evolution, and the ecology of microbial communities in the soil. I have strong research interests to develop new strategies that can help prevent bacterial infectious diseases of plants as well as humans.