Kate O'Connor-Giles

Molecular regulation of synaptic growth

Office Phone: 265-4813

Research Strengths: Development, Plasticity and Repair

Neurons function within neural circuits to regulate behaviors ranging from simple reflexes to learning and memory. Synapses - the connections between neurons and their targets - are the functional units of neural circuits. We are interested in how neurons build synaptic connections and modulate their strength. Synapses comprise a presynaptic active zone that is responsible for the Ca2+ dependent release of neurotransmitter-filled synaptic vesicles in response to action potentials. This signal is received by neurotransmitter receptors that cluster opposite active zones at postsynaptic densities. Synapse formation is a complex process that depends on intercellular communication between pre and postsynaptic cells – often at sites very distant from cell bodies. In fact, a single central neuron can form thousands of synapses and must independently regulate the development of each. Synapses must also maintain the life-long ability to modify their morphology and physiology in response to environmental stimuli and changes in activity levels – modifications that are thought to underlie learning and memory.

Defects in synaptic development and plasticity are associated with a broad range of neurological disorders including developmental disorders such as autism; motor, cognitive and psychological impairments; and neurodegeneration. Thus, the identification and characterization of the molecules that regulate synapse formation and function is key to our understanding of normal neural function and our ability to treat a variety of neurological disorders. The Drosophila larval NMJ is an ideal model system for elucidating the general principles underlying synaptogenesis. In addition to highly amenable genetics, the Drosophila NMJ is readily accessible for imaging and electrophysiological analysis. Importantly, the molecules and mechanisms implicated in synaptogenesis at the Drosophila NMJ are remarkably conserved.

Selected Publications:

Bruckner, J*., Gratz, S*., Slind, J., Geske, R., Cummings, A., Galindo, S., Donohue, L. and O’Connor-Giles, K. (2012). Fife, a Drosophila Piccolo-RIM homolog, promotes active zone organization and neurotransmitter release.J Neurosci. 32(48), 17048-58.
Babaoglan, A.B., K.M. O’Connor-Giles, H. Mistry, A. Schickedanz, B.A. Wilson, and J.B.2009. Skeath. Sanpodo: a context-dependent activator and inhibitor of Notch signaling during asymmetric divisions. 2009 December 15; 136(24): 4089–4098. doi:10.1242/dev.040386
O’Connor-Giles, K.M. and B. Ganetzky. 2008. Satellite Signaling at Synapses. Fly 2:259-61.
O’Connor-Giles, K.M., L.L. Ho, and B. Ganetzky. 2008. Nervous wreck interacts with Thickveins and the endocytic machinery to attenuate retrograde BMP growth signaling during synaptic growth. Neuron 58:507-518.
O’Connor-Giles, K.M. and J.B. Skeath. 2003. Numb inhibits membrane localization of Sanpodo, a four-pass transmembrane protein, to promote asymmetric divisions in Drosophila. Dev. Cell 5:231-43.


Program Welcome Contact Recent News Overview Getting a Degree Graduate Courses Seminars Lecture Series Journal Clubs Directions	Research Strengths Faculty Research Student Research	Admissions Requirements Application Financial Aid Fee Grants Application Status FAQ's Check List Public Policy Program	Resources Current Students Course Pages Course Requirements Forms Alumni Directory The University More Resources	Events Annual Picnic Graduate Fair K-12 Outreach Poster Fair Research Symposium Bio Preview	Undergrad Neurobiology Major Option Undergraduate Courses Research Opportunities Research Awards Research Funds Neuroscience Society Jobs in Science Application	N & PP

Kate O'Connor-Giles Molecular regulation of synaptic growth E-mail: oconnorgiles@wisc.edu Office Phone: 265-4813 Lab Website: O'connor-Giles Laboratory Research Strengths: Development, Plasticity and Repair Neurons function within neural circuits to regulate behaviors ranging from simple reflexes to learning and memory. Synapses - the connections between neurons and their targets - are the functional units of neural circuits. We are interested in how neurons build synaptic connections and modulate their strength. Synapses comprise a presynaptic active zone that is responsible for the Ca2+ dependent release of neurotransmitter-filled synaptic vesicles in response to action potentials. This signal is received by neurotransmitter receptors that cluster opposite active zones at postsynaptic densities. Synapse formation is a complex process that depends on intercellular communication between pre and postsynaptic cells – often at sites very distant from cell bodies. In fact, a single central neuron can form thousands of synapses and must independently regulate the development of each. Synapses must also maintain the life-long ability to modify their morphology and physiology in response to environmental stimuli and changes in activity levels – modifications that are thought to underlie learning and memory. Defects in synaptic development and plasticity are associated with a broad range of neurological disorders including developmental disorders such as autism; motor, cognitive and psychological impairments; and neurodegeneration. Thus, the identification and characterization of the molecules that regulate synapse formation and function is key to our understanding of normal neural function and our ability to treat a variety of neurological disorders. The Drosophila larval NMJ is an ideal model system for elucidating the general principles underlying synaptogenesis. In addition to highly amenable genetics, the Drosophila NMJ is readily accessible for imaging and electrophysiological analysis. Importantly, the molecules and mechanisms implicated in synaptogenesis at the Drosophila NMJ are remarkably conserved. Selected Publications: Bruckner, J., Gratz, S., Slind, J., Geske, R., Cummings, A., Galindo, S., Donohue, L. and O’Connor-Giles, K. (2012). Fife, a Drosophila Piccolo-RIM homolog, promotes active zone organization and neurotransmitter release.J Neurosci. 32(48), 17048-58. Babaoglan, A.B., K.M. O’Connor-Giles, H. Mistry, A. Schickedanz, B.A. Wilson, and J.B.2009. Skeath. Sanpodo: a context-dependent activator and inhibitor of Notch signaling during asymmetric divisions. 2009 December 15; 136(24): 4089–4098. doi:10.1242/dev.040386 O’Connor-Giles, K.M. and B. Ganetzky. 2008. Satellite Signaling at Synapses. Fly 2:259-61. O’Connor-Giles, K.M., L.L. Ho, and B. Ganetzky. 2008. Nervous wreck interacts with Thickveins and the endocytic machinery to attenuate retrograde BMP growth signaling during synaptic growth. Neuron 58:507-518. O’Connor-Giles, K.M. and J.B. Skeath. 2003. Numb inhibits membrane localization of Sanpodo, a four-pass transmembrane protein, to promote asymmetric divisions in Drosophila. Dev. Cell 5:231-43.

Search NTP: UW Home Graduate School Site Map Copyright © 2003 The Board of Regents of the University of Wisconsin System Page Created June 3, 2003 \| Last Updated December 27, 2012 Question or Comments, Please contact the program at ntp@mhub.neuroscience.wisc.edu