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MeCP2 suppresses nuclear microRNA processing and dendritic growth by regulating the DGCR8/Drosha complex.

Authors: Cheng, Tian-Lin  Wang, Zhizhi  Liao, Qiuming  Zhu, Ying  Zhou, Wen-Hao  Xu, Wenqing  Qiu, Zilong 
Citation: Cheng TL, etal., Dev Cell. 2014 Mar 10;28(5):547-60. doi: 10.1016/j.devcel.2014.01.032.
Pubmed: (View Article at PubMed) PMID:24636259
DOI: Full-text: DOI:10.1016/j.devcel.2014.01.032

Loss- and gain-of-function mutations of the X-linked gene MECP2 (methyl-CpG binding protein 2) lead to severe neurodevelopmental disorders in humans, such as Rett syndrome (RTT) and autism. MeCP2 is previously known as a transcriptional repressor by binding to methylated DNA and recruiting histone deacetylase complex (HDAC). Here, we report that MeCP2 regulates gene expression posttranscriptionally by suppressing nuclear microRNA processing. We found that MeCP2 binds directly to DiGeorge syndrome critical region 8 (DGCR8), a critical component of the nuclear microRNA-processing machinery, and interferes with the assembly of Drosha and DGCR8 complex. Protein targets of MeCP2-suppressed microRNAs include CREB, LIMK1, and Pumilio2, which play critical roles in neural development. Gain of function of MeCP2 strongly inhibits dendritic and spine growth, which depends on the interaction of MeCP2 and DGCR8. Thus, control of microRNA processing via direct interaction with DGCR8 represents a mechanism for MeCP2 regulation of gene expression and neural development.


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CRRD Object Information
CRRD ID: 12789709
Created: 2017-02-15
Species: All species
Last Modified: 2017-02-15
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.