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Dissecting the Precise Role of Histone H3 K9 Methylation in Crosstalk with DNA Maintenance Methylation in Mammalian Cells

ABSTRACT: Our study supports a role for H3K9 methylation in promoting DNA methylation, it demonstrates for the first time that DNA maintenance methylation in mammalian cells is to large extent independent on H3K9 methylation. Examination of DNA methylation levels in UHRF1 knock in and wide type mice.

ORGANISM(S): Mus musculus

SUBMITTER: Hao Cheng

PROVIDER: E-GEOD-83884 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dissecting the Precise Role of Histone H3 K9 Methylation in Crosstalk with DNA Maintenance Methylation in Mammalian Cells

Project description:Our study supports a role for H3K9 methylation in promoting DNA methylation, it demonstrates for the first time that DNA maintenance methylation in mammalian cells is to large extent independent on H3K9 methylation.

2016-06-30 | GSE83884 | GEO

Hemi-methylated DNA regulates DNA methylation inheritance through allosteric control of H3 ubiquitylation by UHRF1

Project description:DNA methylation is a heritable chromatin modification essential to mammalian development that functions with histone post-translational modifications to regulate chromatin structure and gene expression programs. The epigenetic inheritance of DNA methylation requires the combined actions of DNMT1 and UHRF1, a histone- and DNA-binding RING E3 ubiquitin ligase that facilitates DNMT1 recruitment to sites of newly replicated DNA through the ubiquitylation of histone H3. UHRF1 binds DNA with modest selectivity towards hemi-methylated CpG dinucleotides (HeDNA); however, the contribution of HeDNA sensing to UHRF1 function remains elusive. Here, we reveal that the interaction of UHRF1 with HeDNA is required for DNA methylation inheritance but is dispensable for chromatin interaction, which is governed by reciprocal positive cooperativity between the UHRF1 histone- and DNA-binding domains. We further show that HeDNA functions as an allosteric regulator of UHRF1 ubiquitin ligase activity, directing ubiquitylation towards multiple lysines on the H3 tail adjacent to the UHRF1 histone-binding site. Collectively, our studies define a highly orchestrated epigenetic control mechanism involving modifications both to histones and DNA that facilitate UHRF1 chromatin targeting, H3 ubiquitylation, and DNA methylation inheritance.

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Dissecting the precise role of H3K9 methylation in crosstalk with DNA maintenance methylation in mammals.

Project description:In mammals it is unclear if UHRF1-mediated DNA maintenance methylation by DNMT1 is strictly dependent on histone H3K9 methylation. Here we have generated an Uhrf1 knockin (KI) mouse model that specifically abolishes the H3K9me2/3-binding activity of Uhrf1. The homozygous Uhrf1 KI mice are viable and fertile, and exhibit ∼10% reduction of DNA methylation in various tissues. The reduced DNA methylation occurs globally in the genome and does not restrict only to the H3K9me2/3 enriched repetitive sequences. In vitro UHRF1 binds with higher affinity to reconstituted nucleosome with hemi-methylated CpGs than that with H3K9me2/3, although it binds cooperatively to nucleosome with both modifications. We also show that the nucleosome positioning affects the binding of methylated DNA by UHRF1. Thus, while our study supports a role for H3K9 methylation in promoting DNA methylation, it demonstrates for the first time that DNA maintenance methylation in mammals is largely independent of H3K9 methylation.

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A histone mimic within DNA Ligase 1 links DNA replication and DNA remethylation: a revised model for the maintenance of DNA methylation by UHRF (RRBS)

Project description:DNA methylation is an essential epigenetic mark in mammals, and its pattern has to be re-established after each round of DNA replication. The protein UHRF1 is known to be necessary for this process, but its mode of action is unclear. Using proteomics, we havefound that a replication factor, DNA Ligase 1 (LIG1), is a direct interactor of UHRF1. The interaction is mediated bythe Tudor domain of UHRF1 and an H3K9-like histone mimic within LIG1. This mimic ismethylated on a conserved lysine by the enzymes G9a and GLP, and outcompetes H3K9me3 for UHRF1 binding. Lastly, the interaction with LIG1 promotes the recruitment of UHRF1 to sites of DNA replication and is required for DNA methylation maintenance. These results clarify UHRF1 activity, identify a new non-histone target of G9a and GLP, and provide the first example of a histone mimic that coordinates DNA replication and DNA remethylation

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Maintenance of DNA methylation in embryonic stem cells depends on the histone H3K9 methyltransferases (K9 KO Methyl-Seq)

Project description:During mammalian development DNA methylation patterns need to be reset in primordial germ cells (PGC) and preimplantation embryos. However, many retro-transposons and imprinted genes are resistant to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that some of these sequences are immune to widespread erasure of DNA methylation in the mouse embryonic stem cells (mESCs) lacking de novo DNA methyltransferases. Persistence of DNA methylation at these loci in mESCs depends on the histone H3K9 methyltransferase Setdb1, as deletion of Setdb1 results in reduction of H3K9me3 and DNA methylation levels concomitant with an increase in 5-hydroxymethylation (5hmC). In addition, depletion of H3K9 methyltransferase G9a leads to genome-wide reduction of DNA methylation but to a lesser extent at the above sequences. Taken together, these data reveal that Setdb1 ensures the fidelity of DNA methylation at specific loci in mESCs, which may reflect mechanisms functioning in vivo during key developmental stages. Examination of genome-wide DNA methylation status in 3 cell types.

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H3K9 methyltransferase G9a negatively regulates UHRF1 transdcription during leukemia cell differentiation.

Project description:Posttranslational modifications of histone N-terminal tails influence the status of chromatin and eventually control the transcriptional outcome of a particular gene. As a histone H3K9 methyltransferase (HMTase) in higher eukaryotes, G9a-mediated transcriptional repression is the major epigenetic silencing machinery. UHRF1 (ubiquitin-like with PHD and ring finger domains I) binds to hemi-methylated DNA and plays essential role in maintenance of DNA methylation by recruiting DNMT1. Here, we provide evidence that UHRF1 is transcriptionally downregulated by H3K9 HMTase G9a. We found that increased expression of G9a along with transcription factor YY1 specifically represses UHRF1 transcription. We uncovered showed that G9a regulates UHRF1-mediated H3K23 ubiquitylation and proper DNA replication maintenance by FACS analysis and propose that H3K9 HMTase G9a is a specific epigenetic regulator of UHRF1.

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