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• W2023387411 abstract "ISSN 1750-1911 Epigenomics (2014) 6(1), 17–19 Regulation of memory acquisition and extinction by TET1 Evaluation of: Kaas GA, Zhong C, Eason DE et al. TET1 controls CNS 5-methylcytosine hydroxylation, active DNA demethylation, gene transcription, and memory formation. Neuron 79, 1086–1093 (2013); Rudenko A, Dawlaty MM, Seo J et al. Tet1 is critical for neuronal activity-regulated gene expression and memory extinction. Neuron 79, 1109–1122 (2013). Accumulating evidence indicates that altered gene expression in response to changes in the environment underlies the plasticity in the brain, including learning and memory. Epigenetic modifications, such as DNA methylation and histone acetylation, have been shown to critically regulate gene transcription, providing a candidate mechanism for synaptic and experience-dependent behavioral plasticity. The dynamic changes of epigenetic modifications (e.g., histone acetylation and deacetylation) play key roles in memory formation and extinction [1]. Generation of methylated cytosine (5mC) in DNA was once considered as a stable modification to silence gene transcription. However, recent studies indicated that DNA methylation may undergo rapid changes in vivo. The teneleven translocation (TET) family enzymes, TET1, TET2 and TET3, catalyze the oxidation of 5mC to 5-hydroxymethylcytosine (5hmC) and thus participate in active DNA demethylation [2,3]. Guo et al. found that in response to neuronal activation, TET1 mediates demethylation of the Fgf1 and the Bdnf promoters in the brain [4]. However, the potential role of TET1 as well as TET1mediated DNA demethylation in memory formation is not clear. Recent work by Kaas et al. revealed that TET1 exerts function in active DNA demethylation, gene transcription and memory formation [5]. They showed that TET1 is expressed in neurons throughout the hippocampus in the brain and stimulation of neuronal activity by KCl or seizure downregulates its transcription in hippocampal neurons. Overexpression of TET1 in the dorsal hippocampus result in a significant decrease in global level of 5mC and an increase of 5hmC, indicating that TET1 effectively promotes DNA demethylation by converting 5mC to 5hmC. In parallel, upregulation of activity-dependent genes involved in neuroplasticity, such as Fos, Arc, Egr1, Homer1 and Ner4a2 was also detected in the hippocampus overexpressing TET1. Moreover, Kaas et al. investigated the behavioral effects of TET1. Overexpression of TET1 in the dorsal hippocampus does not affect locomotion and anxietylike behavior, but significantly impairs long-term conditioned fear memory. Interestingly, the expression of a catalytically inactive mutant of TET1 also affected gene expression and memory formation, raising the question that if TET1 regulates gene expression and memory via both hydroxylase activity-dependent and hydroxylase activity-independent mechanisms. Earlier research by Zhang and colleagues showed that Tet1-knockout mice exhibit impaired hippocampal neurogenesis and hippocampus-dependent spatial memory [6]. Rudenko et al. recently examined another stain of Tet1-knockout mice generated by depleting exon 4 [7]. They found that ablation of TET1 does not change the level of 5mC but leads to a reduction of Highlights from the latest articles in epigenomics" @default.
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• W2023387411 date "2014-02-01" @default.
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• W2023387411 title "Highlights from the latest articles in epigenomics" @default.
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• W2023387411 doi "https://doi.org/10.2217/epi.13.85" @default.
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