Chromatin remodeling inactivates activity genes and regulates neural coding

Science. 2016 Jul 15;353(6296):300-305. doi: 10.1126/science.aad4225.

Abstract

Activity-dependent transcription influences neuronal connectivity, but the roles and mechanisms of inactivation of activity-dependent genes have remained poorly understood. Genome-wide analyses in the mouse cerebellum revealed that the nucleosome remodeling and deacetylase (NuRD) complex deposits the histone variant H2A.z at promoters of activity-dependent genes, thereby triggering their inactivation. Purification of translating messenger RNAs from synchronously developing granule neurons (Sync-TRAP) showed that conditional knockout of the core NuRD subunit Chd4 impairs inactivation of activity-dependent genes when neurons undergo dendrite pruning. Chd4 knockout or expression of NuRD-regulated activity genes impairs dendrite pruning. Imaging of behaving mice revealed hyperresponsivity of granule neurons to sensorimotor stimuli upon Chd4 knockout. Our findings define an epigenetic mechanism that inactivates activity-dependent transcription and regulates dendrite patterning and sensorimotor encoding in the brain.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebellum / physiology*
  • Chromatin Assembly and Disassembly*
  • DNA Helicases / metabolism*
  • Dendrites / physiology*
  • Gene Knockout Techniques
  • Gene Silencing*
  • Genome-Wide Association Study
  • Histones / metabolism
  • Mi-2 Nucleosome Remodeling and Deacetylase Complex / metabolism
  • Mice
  • Mice, Knockout
  • Neurons / physiology*
  • Nucleosomes / metabolism
  • Promoter Regions, Genetic
  • Transcription, Genetic

Substances

  • Histones
  • Nucleosomes
  • Mi-2 Nucleosome Remodeling and Deacetylase Complex
  • Mi-2beta protein, mouse
  • DNA Helicases