To learn better, keep the HAT on.
Long-lasting memories are known to require new transcription. Recent studies have highlighted a role for epigenetic alterations, including histone acetylation, in regulating gene expression. In this issue of Neuron, Alarcón et al. and Korzus et al. use two different mouse models of Rubinstein-Taybi syndrome to elucidate a role for the histone acetyltransferase activity of CREB binding protein (CBP) in long-term memory and plasticity.
Martin
Kelsey C
KC
Department of Psychiatry and Beiobehavioral Sciences, Neuropsychiatric Institute, University of California, Los Angeles 90095, USA.
Sun
Yi E
YE
D000107:Acetylation; D000123:Acetyltransferases / Q000502:physiology*; D000818:Animals; D001522:Behavior, Animal; D050882:CREB-Binding Protein; D002843:Chromatin / Q000378:metabolism; D051548:Histone Acetyltransferases; D006657:Histones / Q000378:metabolism; D007858:Learning / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology; D009687:Nuclear Proteins / Q000502:physiology*; D015518:Rett Syndrome / Q000503:physiopathology; D012415:Rubinstein-Taybi Syndrome / Q000503:physiopathology; D015534:Trans-Activators / Q000502:physiology*
D002843:Chromatin; D006657:Histones; D009687:Nuclear Proteins; D015534:Trans-Activators; D000123:Acetyltransferases; D050882:CREB-Binding Protein; C494364:Crebbp protein, mouse; D051548:Histone Acetyltransferases