Bacterial infection involves a constant tug-of-war between host and pathogen for the essential nutrients of life. Acquisition of the first-row transition metal ion zinc from the host is crucial for the survival and propagation of pathogenic bacteria including Streptococcus pneumoniae. S. pneumoniae is the world’s foremost bacterial pathogen. It is the leading cause of bacterial pneumonia, accounting for 15% of all childhood disease mortalities, and kills more children every year than AIDS, malaria and tuberculosis combined. The primary mechanism used by S. pneumoniae to scavenge zinc from the host is the ABC transporter AdcCB and two zinc-recruiting proteins, AdcA and AdcAII. Disruption of this transporter completely attenuates bacterial virulence. Despite this, how this pathway recognises and transports zinc remains poorly understood. By combining molecular microbiology, structural biology, spectroscopic and biochemical studies the complementary roles of the two zinc-recruiting proteins during in vivo infection is shown. Further, a novel mechanism for zinc binding by AdcA is proposed and its possession of two zinc binding sites, in stark contrast to other bacterial metal ion recruiting proteins, is discussed.
Biography: Christopher McDevitt studied Microbiology and Biochemistry at the University of Queensland, completing his PhD in 2002. During this time, he developed strong interests in membrane transport processes and the roles of metal ions in biological systems. He completed 2 postdoctoral posts at the University of Oxford where he trained in membrane protein purification, biochemistry and biophysics with Prof. Ben Berks and A/Prof. Richard Callaghan. In 2008, he relocated to the University of Adelaide to take up a postdoctoral position in the Research Centre for Infectious Diseases. In 2012, he established his own laboratory and, in 2014, was appointed Deputy Director of the Centre. The McDevitt laboratory is interested in bacterial chemical biology and understanding how inorganic chemical components influence host-pathogen interaction.