Email: Dr. B. E. Staveley
Current teaching links:
Molecular and Developmental Biology (BIOL3530)
One of the most important decisions a cell makes during both developmental and pathological processes is the choice between continued survival and death. For the normal processes of life to occur, cell survival mechanisms must function to oppose cell death. Of special interest is the realization that some proto-oncogenes maintain the balance between cell death and cell survival and that the initiation of cancer may result from the loss of such fine control. Drosophila has become an ideal model organism in which to manipulate programmed cell death.
With this in mind, improvement in the standard "state of being", establishing an enhanced homeostasis, complete with a long and healthy life, would be our ultimate achievement, The objectives of my laboratory's research program involve four closely related goals. Firstly, my research program strives to understand the phenomenon of cell survival and the signaling mechanisms that prevent cell death. Secondly, I would like to develop a particular understanding of the subtlety of the cellular decisions that control and differentiate between cell survival and cell growth. Thirdly, as the akt kinase and it's target foxo are key to the above processes, I hope to identify and characterize additional components of the akt signaling pathway and to discover the extent of the biological consequences of these genes such as anti-starvation mechanisms. Fourthly, due to the fundamental importance of cell death mechanisms in neurodegeneration, we are developing models of neurodegenerative diseases such as Parkinson and Huntington Disease and acting to counteract the consequences of cell death and degeneration.
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.
M'Angale, P.G., and B.E. Staveley, under review. The HtrA2 Drosophila model of Parkinson Disease is suppressed by the pro-survival Bcl-2 Buffy. (Submitted March 26, 2016).
M'Angale, P.G., and B.E. Staveley, under review. The HtrA2 Drosophila model of Parkinson Disease is suppressed b. A loss-of-function Pdxk model of Parkinson Disease in Drosophila can be suppressed by Buffy. (Submitted February 24, 2016).
M'Angale, P.G., and B.E. Staveley, under review. Inhibition of autophagy genes Atg6 and Pi3K59F in dopaminergic neurons decreases lifespan and locomotor ability in Drosophila melanogaster. (Submitted February 16, 2016).
M'Angale, P.G., and B.E. Staveley, revised. The Bcl-2 homologue Buffy rescues [alpha]-synuclein-induced Parkinson disease-like phenotypes in Drosophila. ("Possibly Acceptable" with revision submitted February 10, 2016, second revision March 22, 2016).
Merzetti, E.M., L.A. Dolomount, and B.E. Staveley, revised. The FBXO7 homologue nutcracker and binding partner PI31 in Drosophila melanogaster models of Parkinson Disease. ("Potentially" Accepted with minor revisions, second revision submitted December 17, 2015).
M'Angale, P.G., and B.E. Staveley, 2016. Co-expression of Buffy with Buffy-RNAi produces an intermediate phenotype in the Drosophila eye. Drosophila Information Services 99 (In Press; accepted April 11, 2016).
Merzetti, E.M., and B.E. Staveley, 2016. Altered expression of CG5961, a putative Drosophila melanogaster homologue of FBXO9, provides a new model of Parkinson disease. Genetics and Molecular Research (GMR8579; accepted March 4, 2016).
Slade, J.D., and B.E. Staveley, 2016. Extended longevity and survivorship during amino-acid starvation in a Drosophila Sir2 mutant heterozygote. Genome 57: Epub February 22, 2016. DOI: 10.1139/gen-2015-0213.
Slade, J.D., and B.E. Staveley, 2016. Manipulation of components that control feeding behavior in Drosophila melanogaster increases sensitivity to amino-acid starvation. Genetics and Molecular Research 15 (1): gmr.15017489. DOI: 10.4238/gmr.15017489 (12 pages).
Chavoshi, M.A., and B.E. Staveley, 2016. Inhibition of foxo and minibrain in
dopaminergic neurons can model aspects of Parkinson Disease in Drosophila
melanogaster. Advances in Parkinson’s Disease 5: 1-6. DOI:
Slade, J.D., and B.E. Staveley, 2016. Enhanced survival of Drosophila Akt1 hypomorphs during amino-acid starvation requires foxo. Genome 57(2): 87-93. DOI: 10.1139/gen-2015-0113. Epub November 20, 2015.
Merzetti, E.M., and B.E. Staveley, 2015. spargel, the PGC-1α homologue, in models of Parkinson Disease in Drosophila melanogaster. BioMed Central Neuroscience 16: 70 (8 pages). DOI: 10.1186/s12868-015-0210-2.
Slade, F.A., and B.E. Staveley, 2015. arm-Gal4 inheritance influences development and lifespan in Drosophila melanogaster. Genetics and Molecular Research 14: 12788-12796.
Todd, A.M., and B.E. Staveley, 2015. Pink1 rescues Gal4-induced developmental defects in the drosophila eye. Advances in Parkinson's Disease 4: 43-48.
Slade, J.D., and B.E. Staveley, 2015. Compensatory growth in Drosophila Akt1 mutants. BioMed Central Research Notes 8: 77 (10 pages).
Sheaves, D.W., and B.E. Staveley, 2014. A novel GMR-Gal4 insertion produces a rough eye phenotype. Drosophila Information Services 97: 141-143.
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.