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Activity-Induced MeCP2 Phosphorylation Regulates Retinogeniculate Synapse Refinement.

Christopher P TzengTess WhitwamLisa D BoxerEmmy LiAndrew SilberfeldSara TrowbridgeKevin MeiCindy LinRebecca ShamahEric C GriffithWilliam RenthalChinfei ChenMichael Eldon Greenberg
Published in: bioRxiv : the preprint server for biology (2023)
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder that predominantly affects girls. RTT is caused by loss of function mutations in a single gene MeCP2. Girls with RTT develop normally during their first year of life, but then experience neurological abnormalities including breathing and movement difficulties, loss of speech, and seizures. This study investigates the function of the MeCP2 protein in the brain, and how MeCP2 activity is modulated by sensory experience in early life. Evidence is presented that sensory experience affects MeCP2 function, and that this is required for synaptic pruning in the brain. These findings provide insight into MeCP2 function, and clues as to what goes awry in the brain when the function of MeCP2 is disrupted.
Keyphrases
  • resting state
  • early life
  • white matter
  • functional connectivity
  • multiple sclerosis
  • genome wide
  • oxidative stress
  • brain injury
  • binding protein
  • blood brain barrier
  • transcription factor
  • protein kinase
  • prefrontal cortex