Ken Dawson-Scully Assistant Professor PhD: University of Toronto, Canada (2003) Research interests: Neurobiology of cellular stress and neuroprotection, using live cell imaging, electrophysiology, and behavior genetics. Contact information Office: SC 214 Phone:561-297 0337 (office); 561-297 2782 (lab) Email: ken.dawson-scully@fau.edu

Research Interests:

Since the origin of life, organisms have been exposed to dynamic and unpredictable environments that have bred adaptations to buffer internal physiological functioning from external fluctuations. The evolution of complex nervous systems, and the behaviors they subserve, has played a fundamental role in shaping mechanisms for maintaining homeostasis in the face of environmental perturbations. Adapted animals, such as insects, employ genetic, molecular, and physiological strategies to prevent specific neurological pathologies resulting from stressors such as low oxygen (anoxia), high temperatures (hyperthermia), and high levels of free radicals (oxidative stress). My research program is poised to take advantage of this through the use of a genetically tractable model system, the fruit fly Drosophila melanogaster. In the recent past Drosophila has been used to successfully model a number of human disorders such as Alzheimer’s disease, Parkinson’s disease and obesity. Advantages of the fruit fly include its short life-cycle, high fecundity, sequenced genome and amenability to genetic manipulation. Such characteristics, combined with a general conservation of cellular processes between flies and humans, make Drosophila an ideal system to study cellular pathways associated with neural failure following severe trauma, and to develop novel therapies targeting molecules that contribute to neural dysfunction and cell death/damage. Our goal is to develop novel methods for maintaining both neural function and homeostasis during such instances.

Our research program is divided into three areas of interest.
1) Examination of subcellular mechanisms responsible for cellular homeostasis during stress: Through the use of our live cell imaging facility we are examining the subcellular mechanisms responsible for the protection neurons under anoxic, hyperthermic, and oxidative stress using fluorescent and confocal laser microscopy. To achieve this, we are using genetic and pharmacological manipulations of neuroprotective pathways at the level of a single cell (both spatially and temporally).
2) The investigation of the relationship between neural dysfunction and cell death resulting from cellular stress: Through the integrative use of live cellular imaging, electrophysiology, and behavior genetics, we are investigating the efficacy of pharmacological candidates which interact in molecular pathways underlying the protection of cellular function and prevention of cell death in the presence of anoxia, hyperthermia, and oxidative stress.
3) Genetic screens for novel molecules associated with neural protection: Using standard genetic screening methods, we are attempting to discover mutations and natural alleles that maintain fruit fly behavior and survival in the presence of both acute and prolonged anoxic, hyperthermic, and oxidative stress in order to discover novel genes responsible for neuroprotection.

Publications:

Dawson-Scully K, Armstrong GAB, Kent C, Robertson RM, and Sokolowski MB, 2007. Natural variation in the thermotolerance of neural function and behavior due to a cGMP dependent protein kinase. PLoS ONE: 2(8): e773.

Dawson-Scully K, Lin YQ, Imad M, Marin L, Zhang J, Horne JA, Meinertzhagen IA, Karunanithi S, Zinsmaier KE, and Atwood HL. 2007 Morphological and functional effects of altered Cysteine String Protein at the Drosophila larval neuromuscular junction Synapse Oct; 61(1):1-16. Epub 2006 Nov. [Cover Art].

Douglas S, Dawson-Scully K, and Sokolowski MB. 2005. The neurogenetics and evolution of food-related behaviour. Trends Neurosci. Dec; 28(12):644-52.

Bronk P, Nie ZP, Klose MK, Dawson-Scully K, Zhang JH, Robertson RM, Atwood HL, and Zinsmaier KE. 2005. The multiple functions of Cysteine-string protein analyzed at Drosophila nerve terminals. J Neurosci. 25(9): 2204-2214.

Song W, Ranjan R, Dawson-Scully K, Bronk P, Marin L, Seroude L, Lin YJ, Nie ZP, Atwood HL, Benzer S, and Zinsmaier KE 2002. Presynaptic regulation of neurotransmission in Drosophila by the G protein-coupled receptor Methuselah Neuron 36(1): 105-119.

Bronk P, Wenniger JJ, Dawson-Scully K, Guo XF, Hong S, Atwood HL, and Zinsmaier KE 2001. Drosophila Hsc70-4 is critical for neurotransmitter exocytosis in vivo. Neuron 30(2): 475-488.

Dawson-Scully K, Bronk P, Atwood HL, and Zinsmaier KE 2000. Cysteine-string protein increases the calcium sensitivity of neurotransmitter exocytosis in Drosophila. J Neurosci. 20(16): 6039-6047.

Dawson-Scully K, and Robertson RM. 1998. Heat shock protects synaptic transmission in flight motor circuitry of locusts. NeuroReport 9(11): 2589-2593.

Dawson JW, Dawson-Scully K, Robert D, and Robertson RM. 1997. Forewing asymmetries during auditory avoidance in flying locusts.J. Exp. Biol. 200(17): 2323-2335. [Cover Art]

Robertson RM, Xu H, Shoemaker KL, and Dawson-Scully K. 1996. Exposure to heat shock affects thermosensitivity of the locust flight system. J. Neurobiol. 29(3): 367-383.