Kismet Positively Regulates Glutamate Receptor Localization and Synaptic Transmission at the Drosophila Neuromuscular Junction

被引:15
作者
Ghosh, Rupa [1 ]
Vegesna, Srikar [1 ]
Safi, Ramia [4 ]
Bao, Hong [2 ]
Zhang, Bing [2 ]
Marenda, Daniel R. [1 ,3 ]
Liebl, Faith L. W. [4 ]
机构
[1] Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA
[2] Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA
[3] Drexel Univ, Coll Med, Dept Neurobiol & Anat, Philadelphia, PA 19104 USA
[4] So Illinois Univ, Dept Biol Sci, Edwardsville, IL 62026 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
AXONAL-TRANSPORT DEFECTS; HUMAN CHARGE SYNDROME; IN-VIVO; EPIGENETIC MECHANISMS; BEHAVIORAL PHENOTYPES; ALZHEIMERS-DISEASE; GENE-EXPRESSION; ACTIVE ZONES; PROTEIN; CHD7;
D O I
10.1371/journal.pone.0113494
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
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页数:11
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