MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation.

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ID: 265174
2021
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Abstract
Although embryonic brain development and neurodegeneration have received considerable attention, the events that govern postnatal brain maturation are less understood. Here, we identify the miR-29 family to be strikingly induced during the late stages of brain maturation. Brain maturation is associated with a transient, postnatal period of de novo non-CG (CH) DNA methylation mediated by DNMT3A. We examine whether an important function of miR-29 during brain maturation is to restrict the period of CH methylation via its targeting of Dnmt3a. Deletion of miR-29 in the brain, or knockin mutations preventing miR-29 to specifically target Dnmt3a, result in increased DNMT3A expression, higher CH methylation, and repression of genes associated with neuronal activity and neuropsychiatric disorders. These mouse models also develop neurological deficits and premature lethality. Our results identify an essential role for miR-29 in restricting CH methylation in the brain and illustrate the importance of CH methylation regulation for normal brain maturation.
Reference Key
swahari2021microrna29cell Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Swahari, Vijay;Nakamura, Ayumi;Hollville, Emilie;Stroud, Hume;Simon, Jeremy M;Ptacek, Travis S;Beck, Matthew V;Flowers, Cornelius;Guo, Jiami;Plestant, Charlotte;Liang, Jie;Kurtz, C Lisa;Kanke, Matt;Hammond, Scott M;He, You-Wen;Anton, E S;Sethupathy, Praveen;Moy, Sheryl S;Greenberg, Michael E;Deshmukh, Mohanish;
Journal Cell reports
Year 2021
DOI
S2211-1247(21)00260-6
URL
Keywords
epilepsy autism seizures neurodevelopmental disorders mirna mecp2 ch methylation dnmt3a mir-29 non-cg methylation

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