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Lsh, chromatin remodeling family member, modulates genome-wide cytosine methylation patterns at nonrepeat sequences

ABSTRACT: DNA methylation is critical for normal development and plays important roles in genome organization and transcriptional regulation. Although DNA methyltransferases have been identified, the factors that establish and contribute to genome-wide methylation patterns remain elusive. Here, we report a high-resolution cytosine methylation map of the murine genome modulated by Lsh, a chromatin remodeling family member that has previously been shown to regulate CpG methylation at repetitive sequences. We provide evidence that Lsh also controls genome-wide cytosine methylation at nonrepeat sequences and relate those changes to alterations in H4K4me3 modification and gene expression. Deletion of Lsh alters the allocation of cytosine methylation in chromosomal regions of 50 kb to 2 Mb and, in addition, leads to changes in the methylation profile at the 5′ end of genes. Furthermore, we demonstrate that loss of Lsh promotes—as well as prevents—cytosine methylation. Our data indicate that Lsh is an epigenetic modulator that is critical for normal distribution of cytosine methylation throughout the murine genome. This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: PRJNA142995PRJNA142997PRJNA140163PRJNA142993

ORGANISM(S): Mus musculus

PROVIDER: GSE29395 | GEO | 2011/05/20

SECONDARY ACCESSION(S): PRJNA140163

REPOSITORIES: GEO

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Comprehensive genomic map of cytosine methylation for wild-type (WT) and Lsh-/- mouse embryonic fibroblasts

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Comprehensive genomic map of cytosine methylation for wild-type (WT) and Lsh-/- mouse embryonic fibroblasts

Project description:DNA methylation is critical for normal development and plays important roles in genome organization and transcriptional regulation. Although DNA methyltransferases have been identified, the factors that establish and contribute to genome-wide methylation patterns remain elusive. Here, we report a high-resolution cytosine methylation map of the murine genome modulated by Lsh, a chromatin remodeling family member that has previously been shown to regulate CpG methylation at repetitive sequences. We provide evidence that Lsh also controls genome-wide cytosine methylation at nonrepeat sequences and relate those changes to alterations in H4K4me3 modification and gene expression. Deletion of Lsh alters the allocation of cytosine methylation in chromosomal regions of 50 kb to 2 Mb and, in addition, leads to changes in the methylation profile at the 5′ end of genes. Furthermore, we demonstrate that loss of Lsh promotes—as well as prevents—cytosine methylation. Our data indicate that Lsh is an epigenetic modulator that is critical for normal distribution of cytosine methylation throughout the murine genome. We used microarrays to detail a high-resolution cytosine methylation map of the murine genome modulated by Lsh, a chromatin remodeling family member that has previously been shown to regulate CpG methylation at repetitive sequences To investigate how genome-wide DNA methylation patterns are established in mice and how they may specifically depend on Lsh, we generated a comprehensive genomic map of cytosine methylation for wild-type (WT) and Lsh−/− mouse embryonic fibroblasts (MEFs) using methylated DNA immunoprecipitation (MeDIP) combined with whole-genome tiling microarray. In addition, we generated a histone 3 lysine 4 trimethylation (H3K4me3) chromatin map using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq) and also evaluated genome-wide gene expression using cDNA microarrays

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The chromatin remodeler Lsh modulates genome-wide cytosine hydroxymethylation

Project description:The chromatin remodeler Lsh modulates genome-wide cytosine hydroxymethylation

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The chromatin remodeler Lsh modulates genome-wide cytosine hydroxymethylation

Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. While Tet proteins have been associated to epigenetic repression or activation complexes, our understanding of the molecular mechanisms involved in Tet-mediated regulation of gene transcription remains limited. Here, we showed that Tet directly interact with lymphoid-specific helicase (Lsh), a chromatin remodelling factor belonging to the ISWI family. This specific interaction seems to regulate Tet enzymatic activity since Lsh knock-out leads to a substantial reduction of 5-hydroxymethylation global level in mouse embryonic fibroblasts (MEFs) and in embryonic stem cells (ES). Whole genome sequencing of 5hmC in wild-type versus Lsh knock-out MEFs and ESCs showed that in absence of Lsh some regions of the genome gain while others loose 5hmC marks, with a weak correlation to gene expression changes . We further demonstrated that 5hmC modifications upon Lsh loss are not a direct consequence of 5mC decrease as DhMR (differentially hydroxymethylated regions) did not overlap with DMR (differentially methylated regions) underlying that these modifications occurred at different genomic loci. Altogether, our results suggest that DNA 5-hydroxymethylation and nucleosome folding are linked phenomena, highlighting novel means by which Tet proteins may influence gene regulation.

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Lsh regulates LTR retrotransposon repression independent of Dnmt3b function (RNA-Seq)

Project description:Background: Global DNA methylation contributes to genomic integrity by supressing repeat associated transposition events. Several chromatin factors are required in addition to DNA methyltransferases to maintain DNA methylation at intergenic and satellite repeats. Embryos lacking Lsh, a member of the SNF2 superfamily of chromatin helicases, are hypomethylated. The interaction of Lsh with the de novo methyltransferase, Dnmt3b, facilitates the deposition of DNA methylation at stem cell genes. We wished to determine if a similar targeting mechanism operates to maintain DNA methylation at repetitive sequences. Results: We used HELP-seq to map genome wide DNA methylation patterns in Lsh-/- and Dnmt3b-/- somatic cells. DNA methylation is predominantly lost from specific genomic repeats in Lsh-/- cells: LTR-retrotransposons, LINE-1 repeats and mouse satellites. RNA-seq experiments demonstrate that specific IAP (Intracisternal A-type particle) LTRs and satellites, but not LINE-1 elements, are aberrantly transcribed inLsh-/- cells. LTR hypomethylation in Dnmt3b-/- cells is moderate and hypomethylated repetitive elements (IAP, LINE-1 and satellite) are silent. Chromatin immunoprecipitation (ChIP) indicates that repressed LINE-1 elements gain H3K4me3, but H3K9me3 levels are unaltered in Lsh-/- cells, indicating that DNA hypomethylation alone is not permissive for their transcriptional activation. Mis-expressed IAPs and satellites lose H3K9me3 and gain H3K4me3 in Lsh-/- cells. Conclusions: Our study emphasizes that regulation of repetitive elements by DNA methylation is selective and context dependent. We propose a model where Lsh is specifically required at a precise developmental window to target de novo methylation to repeat sequences, which is subsequently maintained by Dnmt1 in somatic cells to enforce repeat silencing thus contributing to genomic integrity.

2013-12-09 | GSE52477 | GEO

Lsh regulates LTR retrotransposon repression independent of Dnmt3b function (HELP-seq)

2013-12-09 | GSE52476 | GEO