Biomedical Research Education & Training
Faculty Member

Broadie, Kendal S., Ph.D.
Stevenson Professor of Neurobiology
Professor of Pharmacology
Professor of Cell and Developmental Biology
Stevenson Professor of Neurobiology

Lab Url:

Phone Number: (615) 936-3937

Email Address:

Broadie, Kendal's picture
Academic history
B.Sc., University of Oregon
Ph.D., University of Cambridge (England)

Office Address   Mailing Address

6270A MRB III, 465 21st Av S 37232

Box 1634 Sta B 37232-8548

Research Keywords
neurobiology, genetics, genomics, development, synaptogenesis, neurotransmission, synaptic plasticity, behavior, learning & memory, genetic models of human disease, mental retardation, neuromuscular TECHNIQUES: classic and molecular Drosophila genetics, biochemistry, electrophysiology, optical imaging, electron microscopy

Clinical Research Keywords
Intellectual Disabilities, Autism, Fragile X Syndrome

Research Description
What are the molecular mechanisms underlying coordinated movement, integrated behavior, cognition, learning and memory? How does the nervous system circuitry underlying these behaviors develop, and how are these circuits modified by experience? How do these mechanisms go awry in inherited neurological diseases and age-related neurological decline? These questions center around the common themes of information transfer and information storage in cells of the nervous system. My long-term interest has been to understand the fundamental principles of nervous system development, function and plasticity by applying systematic genetic analyses to address these questions.

The primary focus of my laboratory is on the synapse, the specialized intercellular junction which functions as the communication link between neurons, and between neurons and muscle. Chemical synapses mediate the vast majority of communication in the nervous system and exhibit plastic properties underlying the behavioral and cognitive malleability of the brain. Our experimental approach is to use a combination of forward genetics, reverse genetics and functional genomics to identify synaptic genes, generate mutants and then assay mutant phenotypes to elucidate the function of normal synaptic gene products. Our laboratory uses this strategy to investigate three closely related questions: 1) How do synapses develop?, 2) How do synapses function? and 3) How do synapses maintain adaptive plasticity?

Synaptic development involves specifying and constructing the intercellular communication link. The developmental program specifies synaptic partnerships and aligns the presynaptic signaling apparatus with the postsynaptic receptor field. The mature function of the synapse is to translate electrical information into chemical information and back again. This information transfer requires mechanisms to couple an action potential to the fusion of neurotransmitter vesicles, receipt of the signal by a receptors and downstream signaling pathways. Synaptic plasticity is the key to nervous system adaptability, including higher cognitive functions. Plasticity is the process whereby synaptic form and/or function is altered is response to use, to modulate communication either transiently (learning) or permanently (memory). We screen directly for genetic mutants defective in learning/memory and then assay the roles of the mutant genes at the synapse.

A primary interest is to develop models of human neurological diseases linked to inherited synaptic dysfunction. On-going studies focus a model of Fragile X syndrome (FXS), the most common inherited neurological disease which results in cognitive impairment and autism spectrum disorders. Multiple lines of evidence suggest that FXS is caused by defects in synaptic development and plasticity due to inappropriate translational regulation. We are employing many complementary behavioral, electrophysiological, imaging and molecular genetic approaches to study this important disease state. We are particularly interested in activity-dependent mechanisms and the regulation of inhibitory vs. excitatory synapses in central brain circuits.

Our approach to the synapse is multi-disciplinary and requires the marriage of many traditionally distinct fields. Our work involves classical geneticists, molecular biologists, developmental cell biologists, anatomists and electrophysiologists. In the long term, we hope that this work will lead to a greater understanding of nervous system development and function including neural network formation, mechanisms of integrated neuronal communication, higher brain functions including learning and memory, and the cure for synaptic dysfunction arising in inherited neurological diseases.

Clinical Research Description
We are interested in uncovering the molecular and cellular bases of neurological diseases. We are particularly interested in inherited diseases linked to synaptic dysfunction. Our goal is to generate powerful genetic models of targeted diseases and then use a combination of forward genetics, reverse genetics and genomic/proteomic strategies to elucidate underlying molecular defects.

One example is Fragile X Syndrome, the most common cause of inherited mental retardation. This disease is caused by defects in translation regulation within neurons leading to an arrest in the functional development of synapses. We have generated a simple genetic model of this disease, and shown that the model recapitulates the major major disease symptoms (Zhang et al., Cell 2001). We are now exploiting this model to identify interacting genes and proteins that regulate synaptic differentiation.

Another example is a disparate set of inherited neurodegeneration diseases. Our hypothesis is that neuronal apoptosis may be a secondary consequence of progressively impaired synaptic transmission required to maintain cell viability. We are working with both "protein storage diseases" (e.g. Parkinson's Disease) and "lipid storage diseases" (e.g. Niemann Pick Type C) to test this hypothesis. Specifically, we are assaying the synaptic roles of idnetified genes known to mutate to cause the inherited conditions.

Guss, KA, Benson, M, Gubitosi, N, Brondell, K, Broadie, K, Skeath, JB. Expression and function of scalloped during Drosophila development. Dev Dyn, 242(7), 874-85, 2013

Nahm, M, Lee, MJ, Parkinson, W, Lee, M, Kim, H, Kim, YJ, Kim, S, Cho, YS, Min, BM, Bae, YC, Broadie, K, Lee, S. Spartin regulates synaptic growth and neuronal survival by inhibiting BMP-mediated microtubule stabilization. Neuron, 77(4), 680-95, 2013

Rohrbough, J, Kent, KS, Broadie, K, Weiss, JB. Jelly Belly trans-synaptic signaling to anaplastic lymphoma kinase regulates neurotransmission strength and synapse architecture. Dev Neurobiol, 73(3), 189-208, 2013

Staples, J, Broadie, K. The cell polarity scaffold Lethal Giant Larvae regulates synapse morphology and function. J Cell Sci, 126(Pt 9), 1992-2003, 2013

Wei, C, Thatcher, EJ, Olena, AF, Cha, DJ, Perdigoto, AL, Marshall, AF, Carter, BD, Broadie, K, Patton, JG. miR-153 regulates SNAP-25, synaptic transmission, and neuronal development. PLoS One, 8(2), e57080, 2013

Coffee, RL, Williamson, AJ, Adkins, CM, Gray, MC, Page, TL, Broadie, K. In vivo neuronal function of the fragile X mental retardation protein is regulated by phosphorylation. Hum Mol Genet, 21(4), 900-15, 2012

Dani, N, Nahm, M, Lee, S, Broadie, K. A targeted glycan-related gene screen reveals heparan sulfate proteoglycan sulfation regulates WNT and BMP trans-synaptic signaling. PLoS Genet, 8(11), e1003031, 2012

Rushton, E, Rohrbough, J, Deutsch, K, Broadie, K. Structure-function analysis of endogenous lectin mind-the-gap in synaptogenesis. Dev Neurobiol, 72(8), 1161-79, 2012

Siller, SS, Broadie, K. Matrix metalloproteinases and minocycline: therapeutic avenues for fragile X syndrome. Neural Plast, 2012, 124548, 2012

Tessier, CR, Broadie, K. Molecular and genetic analysis of the Drosophila model of fragile X syndrome. Results Probl Cell Differ, 54, 119-56, 2012

Broadie, K, Baumgartner, S, Prokop, A. Extracellular matrix and its receptors in Drosophila neural development. Dev Neurobiol, 2011

Dani, N, Broadie, K. Glycosylated synaptomatrix regulation of trans-synaptic signaling. Dev Neurobiol, 2011

Gatto, CL, Broadie, K. Fragile X mental retardation protein is required for programmed cell death and clearance of developmentally-transient peptidergic neurons. Dev Biol, 356(2), 291-307, 2011

Gatto, CL, Broadie, K. Drosophila modeling of heritable neurodevelopmental disorders. Curr Opin Neurobiol, 2011

Siller, SS, Broadie, K. Neural circuit architecture defects in a Drosophila model of Fragile X syndrome are alleviated by minocycline treatment and genetic removal of matrix metalloproteinase. Dis Model Mech, 2011

Tessier, CR, Broadie, K. The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons. Neurobiol Dis, 41(1), 147-59, 2011 PMCID:3003324

Coffee, RL, Tessier, CR, Woodruff, EA, Broadie, K. Fragile X mental retardation protein has a unique, evolutionarily conserved neuronal function not shared with FXR1P or FXR2P. Dis Model Mech, 3(7-8), 471-85, 2010

Gatto, CL, Broadie, K. Genetic controls balancing excitatory and inhibitory synaptogenesis in neurodevelopmental disorder models. Front Synaptic Neurosci, 2, 4, 2010 PMCID:3059704

Kliman, M, Vijayakrishnan, N, Wang, L, Tapp, JT, Broadie, K, McLean, JA. Structural mass spectrometry analysis of lipid changes in a Drosophila epilepsy model brain. Mol Biosyst, 6(6), 958-66, 2010

Long, AA, Mahapatra, CT, Woodruff, EA, Rohrbough, J, Leung, HT, Shino, S, An, L, Doerge, RW, Metzstein, MM, Pak, WL, Broadie, K. The nonsense-mediated decay pathway maintains synapse architecture and synaptic vesicle cycle efficacy. J Cell Sci, 123(Pt 19), 3303-15, 2010 PMCID:3003324

Nahm, M, Long, AA, Paik, SK, Kim, S, Bae, YC, Broadie, K, Lee, S. The Cdc42-selective GAP rich regulates postsynaptic development and retrograde BMP transsynaptic signaling. J Cell Biol, 191(3), 661-75, 2010 PMCID:3003324

Rohrbough, J, Broadie, K. Anterograde Jelly belly ligand to Alk receptor signaling at developing synapses is regulated by Mind the gap. Development, 137(20), 3523-33, 2010 PMCID:3003324

Vijayakrishnan, N, Phillips, SE, Broadie, K. Drosophila rolling blackout displays lipase domain-dependent and -independent endocytic functions downstream of dynamin. Traffic, 11(12), 1567-78, 2010 PMCID:3003324

Chen, K, Featherstone, DE, Broadie, K. Electrophysiological recording in the Drosophila embryo. J Vis Exp(27), 2009 PMCID:2724028

Featherstone, DE, Chen, K, Broadie, K. Harvesting and preparing Drosophila embryos for electrophysiological recording and other procedures. J Vis Exp(27), 2009 PMCID:2724028

Gatto, CL, Broadie, K. The fragile X mental retardation protein in circadian rhythmicity and memory consolidation. Mol Neurobiol, 39(2), 107-29, 2009 PMCID:2677818

Gatto, CL, Broadie, K. Temporal requirements of the fragile x mental retardation protein in modulating circadian clock circuit synaptic architecture. Front Neural Circuits, 3, 8, 2009 PMCID:2737437

Repicky, S, Broadie, K. Metabotropic glutamate receptor-mediated use-dependent down-regulation of synaptic excitability involves the fragile X mental retardation protein. J Neurophysiol, 101(2), 672-87, 2009 PMCID:2657068

Rushton, E, Rohrbough, J, Broadie, K. Presynaptic secretion of mind-the-gap organizes the synaptic extracellular matrix-integrin interface and postsynaptic environments. Dev Dyn, 238(3), 554-71, 2009 PMCID:2677818

Tessier, CR, Broadie, K. Activity-dependent modulation of neural circuit synaptic connectivity. Front Mol Neurosci, 2, 8, 2009 PMCID:2724028

Vijayakrishnan, N, Woodruff, EA, Broadie, K. Rolling blackout is required for bulk endocytosis in non-neuronal cells and neuronal synapses. J Cell Sci, 122(Pt 1), 114-25, 2009 PMCID:2714403

Bolduc, FV, Bell, K, Cox, H, Broadie, KS, Tully, T. Excess protein synthesis in Drosophila fragile X mutants impairs long-term memory. Nat Neurosci, 11(10), 1143-5, 2008 PMCID:2637405

Gatto, CL, Broadie, K. Temporal requirements of the fragile X mental retardation protein in the regulation of synaptic structure. Development, 135(15), 2637-48, 2008 PMCID:2753511

Long, AA, Kim, E, Leung, HT, Woodruff, E, An, L, Doerge, RW, Pak, WL, Broadie, K. Presynaptic calcium channel localization and calcium-dependent synaptic vesicle exocytosis regulated by the Fuseless protein. J Neurosci, 28(14), 3668-82, 2008 PMCID:2769928

Mohrmann, R, Matthies, HJ, Woodruff, E, Broadie, K. Stoned B mediates sorting of integral synaptic vesicle proteins. Neuroscience, 153(4), 1048-63, 2008 PMCID:2696304

Pan, L, Woodruff, E, Liang, P, Broadie, K. Mechanistic relationships between Drosophila fragile X mental retardation protein and metabotropic glutamate receptor A signaling. Mol Cell Neurosci, 37(4), 747-60, 2008 PMCID:2769928

Phillips, SE, Woodruff, EA, Liang, P, Patten, M, Broadie, K. Neuronal loss of Drosophila NPC1a causes cholesterol aggregation and age-progressive neurodegeneration. J Neurosci, 28(26), 6569-82, 2008 PMCID:2637405

Reeve, SP, Lin, X, Sahin, BH, Jiang, F, Yao, A, Liu, Z, Zhi, H, Broadie, K, Li, W, Giangrande, A, Hassan, BA, Zhang, YQ. Mutational analysis establishes a critical role for the N terminus of fragile X mental retardation protein FMRP. J Neurosci, 28(12), 3221-6, 2008 PMCID:2769928

Tessier, CR, Broadie, K. Drosophila fragile X mental retardation protein developmentally regulates activity-dependent axon pruning. Development, 135(8), 1547-57, 2008 PMCID:2769928

Venkatachalam, K, Long, AA, Elsaesser, R, Nikolaeva, D, Broadie, K, Montell, C. Motor deficit in a Drosophila model of mucolipidosis type IV due to defective clearance of apoptotic cells. Cell, 135(5), 838-51, 2008 PMCID:2649760

Woodruff, EA, Broadie, K, Honegger, HW. Two peptide transmitters co-packaged in a single neurosecretory vesicle. Peptides, 29(12), 2276-80, 2008 PMCID:2637405

Pan, L, Broadie, KS. Drosophila fragile X mental retardation protein and metabotropic glutamate receptor A convergently regulate the synaptic ratio of ionotropic glutamate receptor subclasses. J Neurosci, 27(45), 12378-89, 2007

Huang, F.D., Woodruff, E., Mohrmann, R. and Broadie, K.. Rolling Blackout is acutely required for synaptic vesicle exocytosis . Journal of Neuroscience, 26, 2369-79, 2006

Vijayakrishnan, N, Broadie, K. Temperature-sensitive paralytic mutants: insights into the synaptic vesicle cycle. Biochem Soc Trans, 34(Pt 1), 81-7, 2006

Broadie, K, Pan, L. Translational complexity of the fragile x mental retardation protein: insights from the fly. Mol Cell, 17(6), 757-9, 2005

Rohrbough, J, Broadie, K. Lipid regulation of the synaptic vesicle cycle. Nat Rev Neurosci, 6(2), 139-50, 2005

Zhang, YQ, Broadie, K. Fathoming fragile X in fruit flies. Trends Genet, 21(1), 37-45, 2005

Zhang, YQ, Friedman, DB, Wang, Z, Woodruff, E, Pan, L, O'donnell, J, Broadie, K. Protein Expression Profiling of the Drosophila Fragile X Mutant Brain Reveals Up-regulation of Monoamine Synthesis. Mol Cell Proteomics, 4(3), 278-290, 2005

Bogdanik, L, Mohrmann, R, Ramaekers, A, Bockaert, J, Grau, Y, Broadie, K, Parmentier, ML. The Drosophila metabotropic glutamate receptor DmGluRA regulates activity-dependent synaptic facilitation and fine synaptic morphology. J Neurosci, 24(41), 9105-16, 2004

Broadie, K. Synapse scaffolding: intersection of endocytosis and growth. Curr Biol, 14(19), R853-5, 2004

Broadie, Kendal. Axon pruning: an active role for glial cells. Curr Biol, 14(8), R302-4, 2004

Huang, FD, Matthies, HJ, Speese, SD, Smith, MA, Broadie, K. Rolling blackout, a newly identified PIP2-DAG pathway lipase required for Drosophila phototransduction. Nat Neurosci, 7(10), 1070-8, 2004

Mohrmann, R., Bogdanik, L., Ramaekers, A., Bockaert, J., Grau, Y., Paramentier, M.L.* and Broadie, K.*. The Drosophila metabotrophic glutamate receptor, DmGluRA, regulates activity-dependent synaptic facilitation and fine synaptic morphology. Journal of Neuroscience, 24, 9105-9116, 2004

Pan, L, Zhang, YQ, Woodruff, E, Broadie, K. The Drosophila fragile X gene negatively regulates neuronal elaboration and synaptic differentiation. Curr Biol, 14(20), 1863-70, 2004

Rohrbough, J, Rushton, E, Palanker, L, Woodruff, E, Matthies, HJ, Acharya, U, Acharya, JK, Broadie, K. Ceramidase regulates synaptic vesicle exocytosis and trafficking. J Neurosci, 24(36), 7789-803, 2004 PMCID:2675194

Trotta, Nick, Orso, Genny, Rossetto, Maria Giovanna, Daga, Andrea, Broadie, Kendal. The hereditary spastic paraplegia gene, spastin, regulates microtubule stability to modulate synaptic structure and function. Curr Biol, 14(13), 1135-47, 2004

Trotta, Nick, Rodesch, Chris K, Fergestad, Tim, Broadie, Kendal. Cellular bases of activity-dependent paralysis in Drosophila stress-sensitive mutants. J Neurobiol, 60(3), 328-47, 2004

Zhang, Yong Q, Matthies, Heinrich J G, Mancuso, Joel, Andrews, Hillary K, Woodruff, Elvin, Friedman, David, Broadie, Kendal. The Drosophila fragile X-related gene regulates axoneme differentiation during spermatogenesis. Dev Biol, 270(2), 290-307, 2004

Aravamudan, Bharathi, Broadie, Kendal. Synaptic Drosophila UNC-13 is regulated by antagonistic G-protein pathways via a proteasome-dependent degradation mechanism. J Neurobiol, 54(3), 417-38, 2003

Matthies, Heinrich J G, Broadie, Kendal. Techniques to dissect cellular and subcellular function in the Drosophila nervous system. Methods Cell Biol, 71, 195-265, 2003

Renden, Robert B, Broadie, Kendal. Mutation and activation of Galpha s similarly alters pre- and postsynaptic mechanisms modulating neurotransmission. J Neurophysiol, 89(5), 2620-38, 2003

Rohrbough, Jeffrey, O''Dowd, Diane K, Baines, Richard A, Broadie, Kendal. Cellular bases of behavioral plasticity: establishing and modifying synaptic circuits in the Drosophila genetic system. J Neurobiol, 54(1), 254-71, 2003

Speese, Sean D, Trotta, Nick, Rodesch, Chris K, Aravamudan, Bharathi, Broadie, Kendal. The ubiquitin proteasome system acutely regulates presynaptic protein turnover and synaptic efficacy. Curr Biol, 13(11), 899-910, 2003

Andrews, Hillary K, Zhang, Yong Q, Trotta, Nick, Broadie, Kendal. Drosophila sec10 is required for hormone secretion but not general exocytosis or neurotransmission. Traffic, 3(12), 906-21, 2002

Beumer, Kelly, Matthies, Heinrich J G, Bradshaw, Amber, Broadie, Kendal. Integrins regulate DLG/FAS2 via a CaM kinase II-dependent pathway to mediate synapse elaboration and stabilization during postembryonic development. Development, 129(14), 3381-91, 2002

Broadie, Kendal S, Richmond, Janet E. Establishing and sculpting the synapse in Drosophila and C. elegans. Curr Opin Neurobiol, 12(5), 491-8, 2002

Featherstone, D, Broadie, K. Response: meaningless minis. Trends Neurosci, 25(8), 386-7, 2002

Featherstone, David E, Broadie, Kendal. Wrestling with pleiotropy: genomic and topological analysis of the yeast gene expression network. Bioessays, 24(3), 267-74, 2002

Featherstone, David E, Rushton, Emma, Broadie, Kendal. Developmental regulation of glutamate receptor field size by nonvesicular glutamate release. Nat Neurosci, 5(2), 141-6, 2002

Richmond, Janet E, Broadie, Kendal S. The synaptic vesicle cycle: exocytosis and endocytosis in Drosophila and C. elegans. Curr Opin Neurobiol, 12(5), 499-507, 2002

Rohrbough, Jeffrey, Broadie, Kendal. Electrophysiological analysis of synaptic transmission in central neurons of Drosophila larvae. J Neurophysiol, 88(2), 847-60, 2002

Zhang, Yong Q, Rodesch, Christopher K, Broadie, Kendal. Living synaptic vesicle marker: synaptotagmin-GFP. Genesis, 34(1-2), 142-5, 2002

Bodily, K D, Morrison, C M, Renden, R B, Broadie, K. A novel member of the Ig superfamily, turtle, is a CNS-specific protein required for coordinated motor control. J Neurosci, 21(9), 3113-25, 2001

Featherstone, D E, Davis, W S, Dubreuil, R R, Broadie, K. Drosophila alpha- and beta-spectrin mutations disrupt presynaptic neurotransmitter release. J Neurosci, 21(12), 4215-24, 2001

Fergestad, T, Broadie, K. Interaction of stoned and synaptotagmin in synaptic vesicle endocytosis. J Neurosci, 21(4), 1218-27, 2001

Fergestad, T, Wu, M N, Schulze, K L, Lloyd, T E, Bellen, H J, Broadie, K. Targeted mutations in the syntaxin H3 domain specifically disrupt SNARE complex function in synaptic transmission. J Neurosci, 21(23), 9142-50, 2001

Renden, R, Berwin, B, Davis, W, Ann, K, Chin, C T, Kreber, R, Ganetzky, B, Martin, T F, Broadie, K. Drosophila CAPS is an essential gene that regulates dense-core vesicle release and synaptic vesicle fusion. Neuron, 31(3), 421-37, 2001

Zhang, Y Q, Bailey, A M, Matthies, H J, Renden, R B, Smith, M A, Speese, S D, Rubin, G M, Broadie, K. Drosophila fragile X-related gene regulates the MAP1B homolog Futsch to control synaptic structure and function. Cell, 107(5), 591-603, 2001

Featherstone, D E, Broadie, K. Surprises from Drosophila: genetic mechanisms of synaptic development and plasticity. Brain Res Bull, 53(5), 501-11, 2000

Featherstone, D E, Rushton, E M, Hilderbrand-Chae, M, Phillips, A M, Jackson, F R, Broadie, K. Presynaptic glutamic acid decarboxylase is required for induction of the postsynaptic receptor field at a glutamatergic synapse. Neuron, 27(1), 71-84, 2000

Rodesch, C K, Broadie, K. Genetic studies in Drosophila: vesicle pools and cytoskeleton-based regulation of synaptic transmission. Neuroreport, 11(18), R45-53, 2000

Rohrbough, J, Grotewiel, M S, Davis, R L, Broadie, K. Integrin-mediated regulation of synaptic morphology, transmission, and plasticity. J Neurosci, 20(18), 6868-78, 2000

Zhang, Y, Featherstone, D, Davis, W, Rushton, E, Broadie, K. Drosophila D-titin is required for myoblast fusion and skeletal muscle striation. J Cell Sci, 113 ( Pt 17), 3103-15, 2000

Aravamudan, B, Fergestad, T, Davis, W S, Rodesch, C K, Broadie, K. Drosophila UNC-13 is essential for synaptic transmission. Nat Neurosci, 2(11), 965-71, 1999

Beumer, K J, Rohrbough, J, Prokop, A, Broadie, K. A role for PS integrins in morphological growth and synaptic function at the postembryonic neuromuscular junction of Drosophila. Development, 126(24), 5833-46, 1999

Broadie, K S. Development of electrical properties and synaptic transmission at the embryonic neuromuscular junction. Int Rev Neurobiol, 43, 45-67, 1999

Fergestad, T, Davis, W S, Broadie, K. The stoned proteins regulate synaptic vesicle recycling in the presynaptic terminal. J Neurosci, 19(14), 5847-60, 1999

Rohrbough, J, Pinto, S, Mihalek, R M, Tully, T, Broadie, K. latheo, a Drosophila gene involved in learning, regulates functional synaptic plasticity. Neuron, 23(1), 55-70, 1999

Wu, M N, Fergestad, T, Lloyd, T E, He, Y, Broadie, K, Bellen, H J. Syntaxin 1A interacts with multiple exocytic proteins to regulate neurotransmitter release in vivo. Neuron, 23(3), 593-605, 1999

Zhang, Y Q, Broadie, K. Cloning, mapping and tissue-specific expression of Drosophila clathrin-associated protein AP50 gene. Gene, 233(1-2), 171-9, 1999

Broadie, K. Forward and reverse genetic approaches to synaptogenesis. Curr Opin Neurobiol, 8(1), 128-38, 1998

Broadie, K, Rushton, E, Skoulakis, E M, Davis, R L. Leonardo, a Drosophila 14-3-3 protein involved in learning, regulates presynaptic function. Neuron, 19(2), 391-402, 1997

Baumgartner, S, Littleton, J T, Broadie, K, Bhat, M A, Harbecke, R, Lengyel, J A, Chiquet-Ehrismann, R, Prokop, A, Bellen, H J. A Drosophila neurexin is required for septate junction and blood-nerve barrier formation and function. Cell, 87(6), 1059-68, 1996

Broadie, K S. Regulation of the synaptic vesicle cycle in Drosophila. Biochem Soc Trans, 24(3), 639-45, 1996

Keshishian, H, Broadie, K, Chiba, A, Bate, M. The drosophila neuromuscular junction: a model system for studying synaptic development and function. Annu Rev Neurosci, 19, 545-75, 1996

Prokop, A, Landgraf, M, Rushton, E, Broadie, K, Bate, M. Presynaptic development at the Drosophila neuromuscular junction: assembly and localization of presynaptic active zones. Neuron, 17(4), 617-26, 1996

Auld, V J, Fetter, R D, Broadie, K, Goodman, C S. Gliotactin, a novel transmembrane protein on peripheral glia, is required to form the blood-nerve barrier in Drosophila. Cell, 81(5), 757-67, 1995

Bate, M, Broadie, K. Wiring by fly: the neuromuscular system of the Drosophila embryo. Neuron, 15(3), 513-25, 1995

Broadie, K S. Genetic dissection of the molecular mechanisms of transmitter vesicle release during synaptic transmission. J Physiol Paris, 89(2), 59-70, 1995

Broadie, K, Prokop, A, Bellen, H J, O''Kane, C J, Schulze, K L, Sweeney, S T. Syntaxin and synaptobrevin function downstream of vesicle docking in Drosophila. Neuron, 15(3), 663-73, 1995

Broadie, K., Sweeney, S.T., Keane, J., Niemann, H. and O'Kane, C.J. Targeted expression of tetanus toxin light chain in Drosophila specifically eliminates synaptic transmission and causes behavioral defects. Neuron , 14, 341-351, 1995

Schulze, K L, Broadie, K, Perin, M S, Bellen, H J. Genetic and electrophysiological studies of Drosophila syntaxin-1A demonstrate its role in nonneuronal secretion and neurotransmission. Cell, 80(2), 311-20, 1995

Sweeney, ST, Broadie, K, Keane, J, Niemann, H, O'Kane, CJ. Targeted expression of tetanus toxin light chain in Drosophila specifically eliminates synaptic transmission and causes behavioral defects. Neuron, 14(2), 341-51, 1995

3. Harrison, S.D., Broadie, K., van de Goor, J. and Rubin, G.M. Mutations in the Drosophila Rop gene suggest a function in general secretion and synaptic transmission. Neuron , 13, 555-566, 1994

Broadie, K S. Synaptogenesis in Drosophila: coupling genetics and electrophysiology. J Physiol Paris, 88(2), 123-39, 1994

Broadie, K, Bellen, H J, DiAntonio, A, Littleton, J T, Schwarz, T L. Absence of synaptotagmin disrupts excitation-secretion coupling during synaptic transmission. Proc Natl Acad Sci U S A, 91(22), 10727-31, 1994 PMCID:45095

Harrison, S D, Broadie, K, van de Goor, J, Rubin, G M. Mutations in the Drosophila Rop gene suggest a function in general secretion and synaptic transmission. Neuron, 13(3), 555-66, 1994

Hoch, M, Broadie, K, J??ckle, H, Skaer, H. Sequential fates in a single cell are established by the neurogenic cascade in the Malpighian tubules of Drosophila. Development, 120(12), 3439-50, 1994

Meadows, L A, Gell, D, Broadie, K, Gould, A P, White, R A. The cell adhesion molecule, connectin, and the development of the Drosophila neuromuscular system. J Cell Sci, 107 ( Pt 1), 321-8, 1994

Broadie, K S, Bate, M. Development of larval muscle properties in the embryonic myotubes of Drosophila melanogaster. J Neurosci, 13(1), 167-80, 1993

Broadie, K S, Bate, M. Development of the embryonic neuromuscular synapse of Drosophila melanogaster. J Neurosci, 13(1), 144-66, 1993

Broadie, K, Bate, M. Muscle development is independent of innervation during Drosophila embryogenesis. Development, 119(2), 533-43, 1993

Broadie, K, Bate, M. Innervation directs receptor synthesis and localization in Drosophila embryo synaptogenesis. Nature, 361(6410), 350-3, 1993

Broadie, K, Bate, M. Activity-dependent development of the neuromuscular synapse during Drosophila embryogenesis. Neuron, 11(4), 607-19, 1993

Broadie, K, Sink, H, Van Vactor, D, Fambrough, D, Whitington, P M, Bate, M, Goodman, C S. From growth cone to synapse: the life history of the RP3 motor neuron. Dev Suppl, 227-38, 1993

Broadie, K S, Bate, M. The development of adult muscles in Drosophila: ablation of identified muscle precursor cells. Development, 113(1), 103-18, 1991

Tublitz, N, Brink, D, Broadie, K S, Loi, P K, Sylwester, A W. From behavior to molecules: an integrated approach to the study of neuropeptides. Trends Neurosci, 14(6), 254-9, 1991

Broadie, K S, Sylwester, A W, Bate, M, Tublitz, N J. Immunological, biochemical and physiological analyses of cardioacceleratory peptide 2 (CAP2) activity in the embryo of the tobacco hawkmoth Manduca sexta. Development, 108(1), 59-71, 1990

Postdoctoral Position Available

Postdoctoral Position Details
WE ARE VERY ACTIVELY RECRUITING POSTDOCTORAL RESEARCHERS! We are interested in recruiting cellular and molecular biologists interested in neurobiology, particularly synaptic biology. We are particularly keen to recruit experienced electrophysiologists (patch-clamp, TEVC) and confocal microscopists (live imaging, optogenetics). We are also looking for molecular geneticists with experience in Drosophila or other genetic models (yeast, C. elegans, zebrafish).

We use genetic approaches to study the nervous system, particularly the development, function and plasticity of neuronal synapses. We model many human diseases which involve synaptic dysfunction, including Fragile X syndrome. We use a multidisciplinary approach coupling molecular genetics with neurological techniques including electrophysiology, optical imaging and EM.

If you have an interest, please contact me directly at All inquiries should be accompanied by a CV and statement of specific interests.

Updated Date