The eukaryotic genome is packaged into a highly ordered chromatin structure, with specific domains regulating the transcription patterns of local genes. Hathaway et al. now present a breakthrough technique in the artificial induction of chromatin marks and use this experimental model to test the properties of an induced heterochromatic domain.
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CRISPRepi: a multi-omic atlas for CRISPR-based epigenome editing.
Nucleic Acids Res
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Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
CRISPR-based epigenome editing integrates the precision of CRISPR with the capability of epigenetic mark rewriting, offering a tunable and reversible gene regulation strategy without altering the DNA sequences. Various epigenome editing systems have been developed and applied in different organisms and cell types; however, the detailed information is discrete, making it challenging to evaluate the precision of different editing systems and design the optimal sgRNAs for further functional studies. Herein, we developed CRISPRepi (http://crisprepi.
View Article and Find Full Text PDFAllele-specific DNA demethylation editing leads to stable upregulation of allele-specific gene expression.
iScience
October 2024
Institute of Biochemistry and Technical Biochemistry, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.
Epigenome editing is an emerging technology that allows to rewrite epigenome states and reprogram gene expression. Here, we have developed allele-specific DNA demethylation editing at gene promoters containing an SNP by sgRNA/dCas9 mediated recuitment of TET1. Maximal DNA demethylation (up to 90%) was observed 6 days after transient transfection of the epigenome editors and it was almost stable for 15 days.
View Article and Find Full Text PDFRewriting cellular fate: epigenetic interventions in obesity and cellular programming.
Mol Med
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Department of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Jimo Road 150, Shanghai, 200120, China.
External constraints, such as development, disease, and environment, can induce changes in epigenomic patterns that may profoundly impact the health trajectory of fetuses and neonates into adulthood, influencing conditions like obesity. Epigenetic modifications encompass processes including DNA methylation, covalent histone modifications, and RNA-mediated regulation. Beyond forward cellular differentiation (cell programming), terminally differentiated cells are reverted to a pluripotent or even totipotent state, that is, cellular reprogramming.
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Methods Mol Biol
July 2024
Department of Biochemistry, Institute of Biochemistry and Technical Biochemistry, University of Stuttgart, Stuttgart, Germany.
The introduction of CRISPR/Cas systems has resulted in a strong impulse for the field of gene-targeted epigenome/epigenetic reprogramming (EpiEditing), where EpiEditors consisting of a DNA binding part for targeting and an enzymatic part for rewriting of chromatin modifications are applied in cells to alter chromatin modifications at targeted genome loci in a directed manner. Pioneering studies preceding this era indicated causal relationships of chromatin marks instructing gene expression. The accumulating evidence of chromatin reprogramming of a given genomic locus resulting in gene expression changes opened the field for mainstream applications of this technology in basic and clinical research.
View Article and Find Full Text PDFOncohistones and disrupted development in pediatric-type diffuse high-grade glioma.
Cancer Metastasis Rev
June 2023
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Recurrent, clonal somatic mutations in histone H3 are molecular hallmarks that distinguish the genetic mechanisms underlying pediatric and adult high-grade glioma (HGG), define biological subgroups of diffuse glioma, and highlight connections between cancer, development, and epigenetics. These oncogenic mutations in histones, now termed "oncohistones", were discovered through genome-wide sequencing of pediatric diffuse high-grade glioma. Up to 80% of diffuse midline glioma (DMG), including diffuse intrinsic pontine glioma (DIPG) and diffuse glioma arising in other midline structures including thalamus or spinal cord, contain histone H3 lysine 27 to methionine (K27M) mutations or, rarely, other alterations that result in a depletion of H3K27me3 similar to that induced by H3 K27M.
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