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DisruptofDNA -methylation-dependlonggenerepressinRettsyndrome
aseverneurologdisordwithfeaturofautism.MECP2encodamethyl-DNA -bindproteinthathabeenpropostofunctionasatranscriptrepressor,DisruptoftheMECP2geneleadtoRettsyndromRTT.butdespitnumermousstudiexaminneurongeneexpressinMecp2mutants,noclearmodelhaemergforhowMeCP2proteinregultranscription.Hereweidentifiagenome-widlength-dependincreasingeneexpressinMeCP2mutantmousmodelandhumanRTTbrains.WepresentevidthatMeCP2repressgeneexpressbybindtomethylCA sitewithinlonggenes,andthatinneuronlackMeCP2,decreastheexpressoflonggeneattenuRTT-associcellulardeficits.Inaddition,wefindthatlonggeneasapopularenrichforneuronfunctionandselectexpressinthebrain.ThesefindsuggestthatmutatinMeCP2maicausneurologdysfunctbyspecifdisruptlonggeneexpressinthebrain.
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