Abstract：
:Autism spectrum disorders such as Rett syndrome (RTT) have been hypothesized to arise from defects in experience-dependent synapse maturation. RTT is caused by mutations in MECP2, a nuclear protein that becomes phosphorylated at S421 in response to neuronal activation. We show here that disruption of MeCP2 S421 phosphorylation in vivo results in defects in synapse development and behavior, implicating activity-dependent regulation of MeCP2 in brain development and RTT. We investigated the mechanism by which S421 phosphorylation regulates MeCP2 function and show by chromatin immunoprecipitation-sequencing that this modification occurs on MeCP2 bound across the genome. The phosphorylation of MeCP2 S421 appears not to regulate the expression of specific genes; rather, MeCP2 functions as a histone-like factor whose phosphorylation may facilitate a genome-wide response of chromatin to neuronal activity during nervous system development. We propose that RTT results in part from a loss of this experience-dependent chromatin remodeling.
journal_name
Neuronjournal_title
Neuronauthors
Cohen S,Gabel HW,Hemberg M,Hutchinson AN,Sadacca LA,Ebert DH,Harmin DA,Greenberg RS,Verdine VK,Zhou Z,Wetsel WC,West AE,Greenberg MEdoi
10.1016/j.neuron.2011.08.022subject
Has Abstractpub_date
2011-10-06 00:00:00pages
72-85issue
1eissn
0896-6273issn
1097-4199pii
S0896-6273(11)00775-6journal_volume
72pub_type
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