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The CHD Protein, Kismet, is Important for the Recycling of Synaptic Vesicles during Endocytosis
Journal article   Open access   Peer reviewed

The CHD Protein, Kismet, is Important for the Recycling of Synaptic Vesicles during Endocytosis

Nina K Latcheva, Taylor L Delaney, Jennifer M Viveiros, Rachel A Smith, Kelsey M Bernard, Benjamin Harsin, Daniel R Marenda and Faith L W Liebl
Scientific reports, v 9(1), 19368
18 Dec 2019
DOI: https://doi.org/10.1038/s41598-019-55900-6
PMID: 31852969
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1038/s41598-019-55900-6View
Published, Version of Record (VoR)CC BY V4.0,  Open

Abstract

Acyltransferases - genetics Animals Chromatin Assembly and Disassembly - genetics DNA Helicases - genetics DNA-Binding Proteins - genetics Drosophila melanogaster - genetics Drosophila Proteins - genetics Endocytosis - genetics Histone Deacetylase 1 - genetics Homeodomain Proteins - genetics Humans Neurons - metabolism rab GTP-Binding Proteins - genetics Synaptic Vesicles - genetics Synaptic Vesicles - metabolism Transcription Factors - genetics Transcription Initiation Site - drug effects Vesicular Glutamate Transport Proteins - genetics Vesicular Transport Proteins - genetics
Chromatin remodeling proteins of the chromodomain DNA-binding protein family, CHD7 and CHD8, mediate early neurodevelopmental events including neural migration and differentiation. As such, mutations in either protein can lead to neurodevelopmental disorders. How chromatin remodeling proteins influence the activity of mature synapses, however, is relatively unexplored. A critical feature of mature neurons is well-regulated endocytosis, which is vital for synaptic function to recycle membrane and synaptic proteins enabling the continued release of synaptic vesicles. Here we show that Kismet, the Drosophila homolog of CHD7 and CHD8, regulates endocytosis. Kismet positively influenced transcript levels and bound to dap160 and endophilin B transcription start sites and promoters in whole nervous systems and influenced the synaptic localization of Dynamin/Shibire. In addition, kismet mutants exhibit reduced VGLUT, a synaptic vesicle marker, at stimulated but not resting synapses and reduced levels of synaptic Rab11. Endocytosis is restored at kismet mutant synapses by pharmacologically inhibiting the function of histone deacetyltransferases (HDACs). These data suggest that HDAC activity may oppose Kismet to promote synaptic vesicle endocytosis. A deeper understanding of how CHD proteins regulate the function of mature neurons will help better understand neurodevelopmental disorders.

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14 citations in Web of Science
11 citations in Scopus

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Collaboration types
Domestic collaboration
Web of Science research areas
Neurosciences
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