MeCP2 regulates activity-dependent transcriptional responses in olfactory sensory neurons.

Autor:	Lee W; Department of Cell Biology and Human Anatomy., Yun JM; Department of Food and Nutrition, Kwangju Women's University, Gwang ju 506-713, South Korea and., Woods R; Department of Medical Microbiology and Immunology., Dunaway K; Department of Medical Microbiology and Immunology., Yasui DH; Department of Medical Microbiology and Immunology., Lasalle JM; Department of Medical Microbiology and Immunology, UC Davis Genome Center, University of California at Davis, School of Medicine, Davis, CA 95616, USA, UC Davis MIND Institute, Sacramento, CA 95817, USA., Gong Q; Department of Cell Biology and Human Anatomy, qzgong@ucdavis.edu.
Jazyk:	angličtina
Zdroj:	Human molecular genetics [Hum Mol Genet] 2014 Dec 01; Vol. 23 (23), pp. 6366-74. Date of Electronic Publication: 2014 Jul 09.
DOI:	10.1093/hmg/ddu358
Abstrakt:	During postnatal development, neuronal activity controls the remodeling of initially imprecise neuronal connections through the regulation of gene expression. MeCP2 binds to methylated DNA and modulates gene expression during neuronal development and MECP2 mutation causes the autistic disorder Rett syndrome. To investigate a role for MeCP2 in neuronal circuit refinement and to identify activity-dependent MeCP2 transcription regulations, we leveraged the precise organization and accessibility of olfactory sensory axons to manipulation of neuronal activity through odorant exposure in vivo. We demonstrate that olfactory sensory axons failed to develop complete convergence when Mecp2 is deficient in olfactory sensory neurons (OSNs) in an otherwise wild-type animal. Furthermore, we demonstrate that expression of selected adhesion genes was elevated in Mecp2-deficient glomeruli, while acute odor stimulation in control mice resulted in significantly reduced MeCP2 binding to these gene loci, correlating with increased expression. Thus, MeCP2 is required for both circuitry refinement and activity-dependent transcriptional responses in OSNs. (© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
Databáze:	MEDLINE
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