Whole genome bisulfite sequencing analysis to measure the effect of EHMT2 (G9a, Bat8) on DNA methylation in the mouse embryo at 9.5 dpc
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA658310 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12482685_1.fastq.gz | Fastqsanger.gz | |||
| SRR12482685_2.fastq.gz | Fastqsanger.gz | |||
| SRR12482686_1.fastq.gz | Fastqsanger.gz | |||
| SRR12482686_2.fastq.gz | Fastqsanger.gz | |||
| SRR12482687_1.fastq.gz | Fastqsanger.gz |
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Project description:WGBS analysis was used to map DNA methylation in response to the mutation of Ehmt2 gene at the embryonic age of 9.5 days post coitum.
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Project description:The experiment was designed to interpret transcription changes in embryos that are developmentally delayed due to different genetically induced deficiencies in the Ehmt2 gene encoding the H3K9 methyltransferase EHMT2. The deficiencies included zygotic homozygosity, maternal mutation, and parental (maternal, paternal, and biparental) haploinsufficiencies, and their respective controls. The age of the embryos was between 8.5 and 9.5 dpc to allow collecting somite-stage matched embryos and detect transcriptome changes shortly before the death of homozygous mutant embryos at 10.5 dpc. Analyzing the homozygous mutants in a novel four-way comparison we distinguished differentially expressed genes (DEGs) that are direct effects of the mutation from those that correspond to embryo development. We separated the developmental DEGs that occur regardless of EHMT2 between the 6-and 12-somite stages, and then identified those developmental DEGs that uniquely change in either the normal or the mutant development. Ehmt2 zygotic and maternal mutant embryos display an increased variance, suggesting that EHMT2 is responsible for narrowing the transcriptional noise after gastrulation. Some transposable element classes correlate with genotype, but others correlate with developmental stage. EHMT2 is required for suppressing long noncoding transcripts that initiate in transposable elements predominantly of the ERVK-class. The ERVK promoters of noncanonical imprinted genes in the embryo require EHMT2 for biallelic silencing and DNA methylation. The transcriptome of delayed parental haploinsufficient wild type embryos is normal, consistent with their good survival prospects. Our four-way comparison approach is generally applicable to functional dissection of essential transcriptional regulators during development.
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Project description:G9a (EHMT2) and the G9a-like protein GLP (EHMT1) form a stable G9a/GLP heterodimer in embryonic stem cells and function cooperatively to establish and maintain the abundant repressive H3K9me2 modification, in addition to modifying several non-histone proteins. The G9a-dependent H3K9me2 is implicated in lineage-specific gene silencing and covers large chromosomal domains. While the mechanism of H3K9me2maintenance by G9a/GLP is known, how new patterns of this modification are established is not well understood. With this in mind, we used FLAG affinity purification of G9a under two different stringency conditions (150 and 300 mM NaCl) coupled with mass spectrometry to identify proteins stably associated with G9a/GLP, which could serve as potential recruiters of the complex to unmodified chromatin.
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