Danny Hatters

Many cellular functions are driven by changes in the conformation of proteins; some conformational changes act as molecular switches for regulating normal cellular activities, while other conformational changes are non-normal and result in detrimental outcomes to the cell. The Hatters group is interested in examining how non-normal changes in protein conformation lead to cellular dysfunction and disease. A key area of research is determining how misfolded conformations of mutant Huntingtin cause cellular dysfunction in Huntington's disease.

In collaboration with Andrew Hill's laboratory, the Hatters group is also interested in determining how the prion protein converts to the infectious, pathogenic Scrapie form inside live cells. In addition, they are working to detect conformational changes of kinases in live cellls with Terry Mulhern's laboratory.

Techniques include: biophysical approaches including fluorescence spectroscopy, analytical ultracentrifugation, and circular dichroism spectroscopy to examine the structural properties of proteins and assess how they change conformation. This approach is complemented by studies in mammalian cell culture using primarily confocal microscopy and other fluorescence-based techniques for determining how these different conformations behave in situ.

Danny Hatters Bio

Danny Hatters recently completed his post doc at the Gladstone Institutes/University of California, San Francisco under the mentorship of Dr Karl Weisgraber. There he studied how three variants of apolipoprotein E, apoE2, apoE3 and apoE4 differ in their conformation and biophysical properties as a basis for understanding the mechanisms underlying the elevated risk that the apoE4 isoform confers for Alzheimer's disease. In April 2007, he returned to Melbourne to take up a CR Roper Fellowship position in the Department of Biochemistry and Molecular Biology. He is currently developing his own research program focusing on how protein conformations lead to cellular dysfunction and disease.