Kendal Broadie

ORCID: 0000-0003-3783-6023
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About
Contact & Profiles
Research Areas
  • Neurobiology and Insect Physiology Research
  • Cellular transport and secretion
  • Genetics and Neurodevelopmental Disorders
  • Lipid Membrane Structure and Behavior
  • Neuroscience and Neuropharmacology Research
  • Ubiquitin and proteasome pathways
  • Retinal Development and Disorders
  • Autism Spectrum Disorder Research
  • Invertebrate Immune Response Mechanisms
  • Congenital heart defects research
  • Photoreceptor and optogenetics research
  • Insect and Arachnid Ecology and Behavior
  • Genetics, Aging, and Longevity in Model Organisms
  • Mitochondrial Function and Pathology
  • RNA modifications and cancer
  • Plant and Biological Electrophysiology Studies
  • Signaling Pathways in Disease
  • Developmental Biology and Gene Regulation
  • Lysosomal Storage Disorders Research
  • Physiological and biochemical adaptations
  • CRISPR and Genetic Engineering
  • Silk-based biomaterials and applications
  • Axon Guidance and Neuronal Signaling
  • RNA Research and Splicing
  • Glycosylation and Glycoproteins Research

John F. Kennedy Center for the Performing Arts
2016-2025

Vanderbilt University Medical Center
2016-2025

Vanderbilt University
2015-2024

Kennedy Center
2018-2024

Allen Institute for Brain Science
2019-2021

Vanderbilt Health
2016-2020

Chinese Academy of Sciences
2008

Institute of Genetics and Developmental Biology
2008

National Cancer Institute
2004

Frederick National Laboratory for Cancer Research
2004

Synaptotagmin is an integral synaptic vesicle protein proposed to be involved in Ca(2+)-dependent exocytosis during transmission. Null mutations synaptotagmin have been made Drosophila, and the protein's vivo function has assayed at neuromuscular synapse. In absence of synaptotagmin, transmission dramatically impaired but not abolished. null mutants, evoked release decreased by a factor 10. Moreover, fidelity excitation-secretion coupling so that given stimulus generates more variable amount...

10.1073/pnas.91.22.10727 article EN Proceedings of the National Academy of Sciences 1994-10-25

Abstract Critical periods are temporally-restricted, early-life windows when sensory experience remodels synaptic connectivity to optimize environmental input. In the Drosophila juvenile brain, critical period drives synapse elimination, which is transiently reversible. Within olfactory neuron (OSN) classes synapsing onto single projection neurons extending brain learning/memory centers, we find glia mediate experience-dependent pruning of OSN glomeruli downstream odorant exposure. We glial...

10.1038/s41598-024-59942-3 article EN cc-by Scientific Reports 2024-04-20

A Drosophila forward genetic screen for mutants with defective synaptic development identified bad reception ( brec ). Homozygous are embryonic lethal, paralyzed, and show no detectable transmission at the glutamatergic neuromuscular junction (NMJ). Genetic mapping, complementation tests, genomic sequencing that mutations disrupt a previously uncharacterized ionotropic glutamate receptor subunit, named here “GluRIID.” GluRIID is expressed in postsynaptic domain of NMJ, as well widely...

10.1523/jneurosci.4201-04.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-03-23

Fragile X Syndrome (FraX) is a broad-spectrum neurological disorder with symptoms ranging from hyperexcitability to mental retardation and autism. Loss of the fragile 1 (fmr1) gene product, mRNA-binding translational regulator FMRP, causes structural over-elaboration dendritic axonal processes, as well functional alterations in synaptic plasticity at maturity. It unclear, however, whether FraX primarily disease development, or both: distinction that vital for engineering intervention...

10.1242/dev.015867 article EN Development 2008-03-06
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