Deleting HDAC3 rescues long-term memory impairments induced by disruption of the neuron-specific chromatin remodeling subunit BAF53b
Year: 2018
Type: preprint
Abstract: Multiple epigenetic mechanisms, including histone acetylation and nucleosome remodeling, are known to be involved in long-term memory formation. Enhancing histone acetylation by deleting histone deacetylases, like HDAC3, typically enhances long-term memory formation. In contrast, disrupting nucleosome remodeling by blocking the neuron-specific chromatin remodeling subunit BAF53b impairs long-term memory. Here, we show that deleting HDAC3 can ameliorate the impairments in both long-term memory and synaptic plasticity caused by BAF53b mutation. This suggests a dynamic interplay exists between histone acetylation/deacetylation and nucleosome remodeling mechanisms in the regulation of memory formation.
Source: Learning & Memory
Authors: Guanhua Shu, Enikö A. Kramár, Alberto J. López, Grace Huynh, Marcelo A. Wood, Janine L. Kwapis
Institution: University of California, Irvine
Language: English
Topic: Memory and Neural Mechanisms
Subfield: Cognitive Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: diamond
Awards: G1094462540, G3241705315, Epigenetic repression of synaptic plasticity and memory in the aging brain, G420710294, Exercise-induced epigenetic mechanisms underlying neuronal plasticity and cognition, Epigenetic regulation of the circadian gene Per1 in age-related memory impairments, Role of neuron-specific nucleosome remodeling in intellectual disability, G6125851273, G7823823341, G8096620355, G8193734662
OpenAlex ID: W2793445472