Journal article
Epigenetic crosstalk: Pharmacological inhibition of HDACs can rescue defective synaptic morphology and neurotransmission phenotypes associated with loss of the chromatin reader Kismet
Molecular and cellular neurosciences, v 87
Mar 2018
PMID: 29249293
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
We are beginning to appreciate the complex mechanisms by which epigenetic proteins control chromatin dynamics to tightly regulate normal development. However, the interaction between these proteins, particularly in the context of neuronal function, remains poorly understood. Here, we demonstrate that the activity of histone deacetylases (HDACs) opposes that of a chromatin remodeling enzyme at the Drosophila neuromuscular junction (NMJ). Pharmacological inhibition of HDAC function reverses loss of function phenotypes associated with Kismet, a chromodomain helicase DNA-binding (CHD) protein. Inhibition of HDACs suppresses motor deficits, overgrowth of the NMJ, and defective neurotransmission associated with loss of Kismet. We hypothesize that Kismet and HDACs may converge on a similar set of target genes in the nervous system. Our results provide further understanding into the complex interactions between epigenetic protein function in vivo.
•Pharmacological inhibition of HDAC function suppresses decreased kismet phenotypes.•Our data suggests dynamic interactions between epigenetic readers and erasers.•We hypothesize Kismet and HDAC function antagonistically on same target genes.
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Details
- Title
- Epigenetic crosstalk: Pharmacological inhibition of HDACs can rescue defective synaptic morphology and neurotransmission phenotypes associated with loss of the chromatin reader Kismet
- Creators
- Nina K. Latcheva - Drexel UniversityJennifer M. Viveiros - Drexel UniversityEdward A. Waddell - Drexel UniversityPhuong T.T. Nguyen - Drexel UniversityFaith L.W. Liebl - Southern Illinois University EdwardsvilleDaniel R. Marenda - Drexel University
- Publication Details
- Molecular and cellular neurosciences, v 87
- Publisher
- Elsevier
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biology
- Web of Science ID
- WOS:000428361200009
- Scopus ID
- 2-s2.0-85039443528
- Other Identifier
- 991019201218504721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences