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
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