Email: Dr. B. E. Staveley
Current teaching links:
One of the most important decisions a cell can make during both developmental and pathological processes is to choose between continued survival and death. For the normal processes of life to occur, cell survival mechanisms must function to oppose cell death. The mechanisms that distinguish between cell death and cell survival and between aspects of cell growth, the increase in cell size and number, are of fundamental importance to many aspects of biology. The origins of many human diseases may be due to errors in these basic biological functions. Drosophila has become an ideal model organism in which to manipulate programmed cell death.
1) to understand the phenomenon of cell survival and the signaling mechanisms that prevent cell death 2) to develop an understanding of the subtle cellular decisions that control and differentiate between cell survival and cell growth 3) to identify and characterize additional components of the akt signaling pathway especially the biologically significant transcriptional targets of foxo, and to discover the extent of the biological consequences of these genes 4) to develop models of neurodegenerative diseases such as Parkinson's disease
Staveley B.E., 2014. Drosophila Models of Parkinson Disease (Chapter 20) in Movement Disorders: Genetics and Models, Second Edition, Mark S. LeDoux (Ed.) (published October 29, 2014).
Lipsett, D.B., and B.E. Staveley, 2014. A blueberry extract supplemented diet partially re-stores [alpha]-synuclein-dependent lifespan loss and developmental defects in Drosophila. Advances in Parkinson's Disease 3: 3-9.
McGuire, M.K., A.D.S. Grant, and B.E. Staveley, 2013. Chronic exposure to tunicamycin during development has little effect upon the eyes of GMR-Gal4 UAS-lacZ males. Drosophila Information Services 96: 153-155.
Merzetti, E.M., and B.E. Staveley, 2013. Mitochondrial dynamics in degenerative disease and disease models. Neuroscience Discovery 1: 8 (12 pages).
Todd, A.M., and B.E. Staveley, 2013. Pink1and parkin demonstrate multifaceted roles when co-expressed with Foxo. Advances in Parkinson's Disease 2: 5-10.
Merzetti, E.M., C.B. Connors, and B.E. Staveley, 2013. Thinking inside the box: Drosophila F-box protein models of human disease. Journal of Biology 3: 7-14.
M'Angale, P.G., and B.E. Staveley, 2012. Effects of alpha-synuclein expression in the developing Drosophila eye. Drosophila Information Services 95: 85-89.
Todd, A.M., and B.E. Staveley, 2012. Expression of Pink1 with alpha-synuclein in the dopaminergic neurons of Drosophila leads to increases in both lifespan and healthspan. Genetics and Molecular Research 11:1497-502.
Staveley B.E., 2012. Successes of Modelling Parkinson Disease in Drosophila, Mechanisms in Parkinson's Disease - Models and Treatments, Juliana Dushanova (Ed.), ISBN: 978-953-307-876-2, InTech, Available from: http://www.intechopen.com/source/pdfs/27853/InTech-Successes_of_modelling_parkinson_disease_in_drosophila.pdf.
Woodman, P.N., A.M.Todd, and B.E. Staveley, 2011. Eyer: Automated counting of ommatidia using image processing techniques. Drosophila Information Services 94: 142-145.
Mawhinney, R.M.S., and B.E. Staveley, 2011. Expression of GFP can influence aging and climbing ability in Drosophila. Genetics and Molecular Research 10: 494-505.
Todd, A.M., and B.E. Staveley, 2010. Co-expression of a-synuclein in Drosophila dopaminergic neurons does not affect lifespan reduction resulting from PI3K overexpression. Drosophila Information Services 93: 21-23.
MacDonald, J.M., J.N. Moores, and B.E. Staveley, 2008. Microchaetae density is not greatly influenced by the overexpression of akt. Drosophila Information Services 91: 108-110.
Todd, A.M., and B.E. Staveley, 2008. Pink1 suppresses alpha-synuclein
induced phenotypes in a Drosophila model of Parkinson disease. Genome 51:
Moores, J.N., S. Roy, D.W. Nicholson and B.E. Staveley, 2008. Huntingtin
interacting protein 1 can regulate neurogenesis in Drosophila. European
Journal of Neuroscience 28: 599-609.
Kramer, J.M., J.D. Slade, and B.E. Staveley, 2008. foxo is required for
resistance to amino acid starvation in Drosophila. Genome 51: 668-672.
Slade, J.D., and B.E. Staveley, 2007. Comparison of somatic clones of the eye
in the analysis of cell growth. Drosophila Information Services 90: 151-156.
Mitchell, K.J., and B.E. Staveley, 2006. Protocol for the detection and
analysis of cell death in the adult Drosophila brain. Drosophila Information
Services 89: 118-122.
Haywood, A.F.M., and B.E. Staveley, 2006. Mutant alpha-synuclein-induced
degeneration is reduced by parkin in a fly model of Parkinson's disease.
Genome 49: 505-510.
Slade, J.D., J.M. Kramer, and B.E. Staveley, 2005. A novel luciferase assay
for the quantification of insulin signaling in Drosophila. Drosophila
Information Services 88: 118-122.
Staveley, B.E., 2005. Life and Death in the Staveley Lab. The Genetics
Society of Canada Bulletin 36: 97-98.
Todd, A.M., and B.E. Staveley, 2004. Novel assay and analysis for measuring
climbing ability in Drosophila. Drosophila Information Services 87: 101-107.
Haywood, A.F.M., and B.E. Staveley, 2004. parkin counteracts symptoms in a
Drosophila model of Parkinson's disease. BioMed Central Neuroscience 5: 14.
Saunders, L.D., A.F.M. Haywood, and B.E. Staveley, 2003. Overexpression of
phosphatidylinositol 3-OH kinase (PI3K) in dopaminergic neurons dramatically
reduces life span and climbing ability in Drosophila melanogaster. Drosophila
Information Services 86: 107-112.
Kramer, J.M., J.T. Davidge, J.M. Lockyer, and B.E. Staveley, 2003. Expression
of Drosophila foxo regulates growth and can phenocopy starvation. BioMed
Central Developmental Biology 3: 5.
Kramer, J.M., and B.E. Staveley, 2003. GAL4 causes developmental defects and
apoptosis when expressed in the developing eye of Drosophila melanogaster.
Genetics and Molecular Research 2: 43-47.
Haywood, A.F.M., L.D. Saunders, and B.E. Staveley, 2002. dopa
decarboxylase(Ddc)-GAL4 dramatically reduces life span. Drosophila Information Services 85: 42-45.