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      A timely, user-friendly analysis of the mouse DNA methylome

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      1 , 2 , 3 , 4 ,
      Cell Genomics
      Elsevier

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          Abstract

          Mouse models are widely used in biomedical sciences and in epigenetic studies, yet a simple way to interrogate the mouse DNA methylation was lacking. In this issue of Cell Genomics, Zhou et al. 1 describe a mouse DNA methylation microarray to simplify epigenomic analysis.

          Abstract

          Mouse models are widely used in biomedical sciences and in epigenetic studies, yet a simple way to interrogate the mouse DNA methylation was lacking. In this issue of Cell Genomics, Zhou et al. describe a mouse DNA methylation microarray to simplify epigenomic analysis.

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          Most cited references10

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          DNA methylation aging clocks: challenges and recommendations

          Epigenetic clocks comprise a set of CpG sites whose DNA methylation levels measure subject age. These clocks are acknowledged as a highly accurate molecular correlate of chronological age in humans and other vertebrates. Also, extensive research is aimed at their potential to quantify biological aging rates and test longevity or rejuvenating interventions. Here, we discuss key challenges to understand clock mechanisms and biomarker utility. This requires dissecting the drivers and regulators of age-related changes in single-cell, tissue- and disease-specific models, as well as exploring other epigenomic marks, longitudinal and diverse population studies, and non-human models. We also highlight important ethical issues in forensic age determination and predicting the trajectory of biological aging in an individual.
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            Global epigenomic reconfiguration during mammalian brain development.

            DNA methylation is implicated in mammalian brain development and plasticity underlying learning and memory. We report the genome-wide composition, patterning, cell specificity, and dynamics of DNA methylation at single-base resolution in human and mouse frontal cortex throughout their lifespan. Widespread methylome reconfiguration occurs during fetal to young adult development, coincident with synaptogenesis. During this period, highly conserved non-CG methylation (mCH) accumulates in neurons, but not glia, to become the dominant form of methylation in the human neuronal genome. Moreover, we found an mCH signature that identifies genes escaping X-chromosome inactivation. Last, whole-genome single-base resolution 5-hydroxymethylcytosine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions that are CG-demethylated and activated in the adult brain and that CG demethylation at these hmC-poised loci depends on Tet2 activity.
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              Validation of a DNA methylation microarray for 850,000 CpG sites of the human genome enriched in enhancer sequences

              Aim: DNA methylation is the best known epigenetic mark. Cancer and other pathologies show an altered DNA methylome. However, delivering complete DNA methylation maps is compromised by the price and labor-intensive interpretation of single nucleotide methods. Material & methods: Following the success of the HumanMethylation450 BeadChip (Infinium) methylation microarray (450K), we report the technical and biological validation of the newly developed MethylationEPIC BeadChip (Infinium) microarray that covers over 850,000 CpG methylation sites (850K). The 850K microarray contains >90% of the 450K sites, but adds 333,265 CpGs located in enhancer regions identified by the ENCODE and FANTOM5 projects. Results & conclusion: The 850K array demonstrates high reproducibility at the 450K CpG sites, is consistent among technical replicates, is reliable in the matched study of fresh frozen versus formalin-fixed paraffin-embeded samples and is also useful for 5-hydroxymethylcytosine. These results highlight the value of the MethylationEPIC BeadChip as a useful tool for the analysis of the DNA methylation profile of the human genome.
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                Author and article information

                Contributors
                Journal
                Cell Genom
                Cell Genom
                Cell Genomics
                Elsevier
                2666-979X
                13 July 2022
                13 July 2022
                13 July 2022
                : 2
                : 7
                : 100153
                Affiliations
                [1 ]Josep Carreras Leukaemia Research Institute (IJC), Badalona, Barcelona, Catalonia, Spain
                [2 ]Centro de Investigacion Biomedica en Red Cancer (CIBERONC), 28029 Madrid, Spain
                [3 ]Institucio Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Catalonia, Spain
                [4 ]Physiological Sciences Department, School of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Catalonia, Spain
                Author notes
                []Corresponding author mesteller@ 123456carrerasresearch.org
                Article
                S2666-979X(22)00090-8 100153
                10.1016/j.xgen.2022.100153
                9903646
                36776781
                06f9f714-0bd2-4338-8033-273b34dfb429
                © 2022 The Author(s)

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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