Kismet positively regulates glutamate receptor localization and synaptic transmission at the Drosophila neuromuscular junction
Autor: | Daniel R. Marenda, Rupa Ghosh, Ramia Safi, Hong Bao, Srikar Vegesna, Faith L.W. Liebl, Bing Zhang |
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Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
lcsh:Medicine
Biochemistry Synaptic Transmission Ion Channels Chromodomain 0302 clinical medicine Postsynaptic potential Drosophila Proteins lcsh:Science Evoked Potentials Motor Neurons 0303 health sciences Multidisciplinary Chromosome Biology Motor Evoked Potentials Muscles Glutamate receptor Anatomy Immunohistochemistry Chromatin Nucleosomes Cell biology DNA-Binding Proteins medicine.anatomical_structure Receptors Glutamate Larva Epigenetics Drosophila Glutamatergic synapse Locomotion Research Article Neuromuscular Junction Neurophysiology Neurotransmission Biology Neuromuscular junction Molecular Genetics 03 medical and health sciences Glutamatergic Genetics medicine Animals 030304 developmental biology Cell Nucleus Homeodomain Proteins fungi lcsh:R DNA Helicases Biology and Life Sciences Proteins Cell Biology Ligand-Gated Ion Channels Motor neuron Chromatin Assembly and Disassembly Cellular Neuroscience Synapses lcsh:Q 030217 neurology & neurosurgery Developmental Biology Neuroscience Synaptic Plasticity |
Zdroj: | PLoS ONE, Vol 9, Iss 11, p e113494 (2014) PLoS ONE |
ISSN: | 1932-6203 |
Popis: | The Drosophila neuromuscular junction (NMJ) is a glutamatergic synapse that is structurally and functionally similar to mammalian glutamatergic synapses. These synapses can, as a result of changes in activity, alter the strength of their connections via processes that require chromatin remodeling and changes in gene expression. The chromodomain helicase DNA binding (CHD) protein, Kismet (Kis), is expressed in both motor neuron nuclei and postsynaptic muscle nuclei of the Drosophila larvae. Here, we show that Kis is important for motor neuron synaptic morphology, the localization and clustering of postsynaptic glutamate receptors, larval motor behavior, and synaptic transmission. Our data suggest that Kis is part of the machinery that modulates the development and function of the NMJ. Kis is the homolog to human CHD7, which is mutated in CHARGE syndrome. Thus, our data suggest novel avenues of investigation for synaptic defects associated with CHARGE syndrome. |
Databáze: | OpenAIRE |
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