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RRBS (Reduced Representation Bisulfite Sequencing) of Egr1-/- and Tet1-/- mouse frontal cortex

ABSTRACT: RRBS (Reduced Representation Bisulfite Sequencing) of Egr1-/- and Tet1-/- mouse frontal cortex

PROVIDER: PRJNA428509 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6441200_1.fastq.gz	Fastqsanger.gz
	SRR6441200_2.fastq.gz	Fastqsanger.gz
	SRR6441210_1.fastq.gz	Fastqsanger.gz
	SRR6441210_2.fastq.gz	Fastqsanger.gz
	SRR6441220_1.fastq.gz	Fastqsanger.gz

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RRBS (Reduced Representation Bisulfite Sequencing) of Egr1-/- and Tet1-/- mouse frontal cortex

Project description:We performed methylome profiling for mouse frontal cortex tissues derived from 6~8 week old Egr1-/- and Tet1-/- mice.

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RNA-seq of Egr1-/- and Tet1-/- mouse frontal cortex

Project description:We performed transcriptome profiling for frontal cortex tissues derived from 6~8 week old Egr1-/- and Tet1-/- mice.

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RNA-seq of Egr1-/- and Tet1-/- mouse frontal cortex

Project description:RNA-seq of Egr1-/- and Tet1-/- mouse frontal cortex

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Egr1 Recruits Tet1 to Shape the Brain Methylome during Early Postnatal Development

Project description:Early growth response gene-1 (Egr1) is a critical transcription factor involved in many important biological processes, including neuronal plasticity and memory formation. With a rapid increase in expression during the first few weeks after birth, Egr1 controls the selection, maturation and functional integration of newborn neurons. The regulation of Egr1-mediated gene expression has been shown to be under methylation control. However, Egr1 target sites and their epigenetic regulation in the nervous system remains largely unknown. In this study, we performed ChIP-seq for EGR1 in mouse frontal cortex and identified a large number of EGR1 binding sites with their cell-type specific methylation patterns established during postnatal frontal cortex development. More specifically, the CpG dinucleotides within these EGR1 binding sites become hypo-methylated in mature neurons but remain heavily methylated in glia. We further demonstrated that EGR1 recruits a DNA demethylase TET1 to remove DNA methylation at EGR1 binding sites and activate downstream genes. In addition, we found that the frontal cortexes from knockout mice with the loss of Egr1 or Tet1 share strikingly similar profiles in both gene expression and DNA methylation. In summary, our study reveals Egr1 as a key mediator for gene-environment interactions shaping brain methylome together with Tet1 during early postnatal development and provides an important new insight into how early life experience may shape the brain methylome. This SuperSeries is composed of the SubSeries listed below.

2019-07-25 | GSE108768 | GEO

Genome-wide maps of TET1 binding in mouse frontal cortex

Project description:With anti-TET1 immunoprecipitated chromatin from mouse frontal cortices, we generated TET1 binding maps with 4496 high-confidence peaks and approximately 90% of TET1 peaks were within intergenic regions.

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Tet1 is a tumor suppressor of hematopoietic maligancy [RRBS]

Project description:Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and causes enhanced Pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed reduced representative bisulfite sequencing (RRBS) of DNA from WT and Tet1 KO LSK cells. DNA methylation sequencing was performed and analyzed using an enhanced reduced representation (ERRBS) methodology as previously described. DNA was extracted from purified LSK cells of 6-month old WT and Tet1 KO mice, Bisulphite treatment was performed using the EZ DNA Methylation Kit (Zymo Research). Libraries were amplified according to illumina protocols and sequenced on an Illumina HiSeq2500 machine DNA methylation profiling of LSK cells in WT and Tet1 KO mice.

2015-04-12 | E-GEOD-65919 | biostudies-arrayexpress

Reduced representation bisulfite sequencing (RRBS) of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO), and Tet1-/-:Tet2-/-:Tet3-/- (TKO) murine embryonic stem under normal culture conditions.

Project description:Reduced representation bisulfite sequencing (RRBS) of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO), and Tet1-/-:Tet2-/-:Tet3-/- (TKO) murine embryonic stem under normal culture conditions.

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Genome-wide maps of TET1 binding in mouse frontal cortex

Project description:Genome-wide maps of TET1 binding in mouse frontal cortex

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Genome-wide maps of EGR1 binding in mouse frontal cortex

Project description:With anti-EGR1 immunoprecipitated chromatin from mouse prefrontal cortices, we generated EGR1 binding maps with 12, 014 high-confidence peaks. Approximately 81% of EGR1 peaks were within genic regions or nearby promoters, and over 45% EGR1 peaks were in the proximal promoter regions within 1 kb from transcription starting sites.

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Role of Tet1 in genomic imprinting erasure [RRBS-PGC]

Project description:Genomic imprinting is an allele-specific gene expression system important for mammalian development and function. The molecular basis of genomic imprinting is allele-specific DNA methylation 2. While it is well known that the de novo DNA methyltransferases Dnmt3a/b are responsible for the establishment of genomic imprinting, how the methylation mark is erased during primordial germ cell (PGC) reprogramming remains a mystery. Here we report that Tet1 plays a critical role in the erasure of genomic imprinting. We show that despite their identical genotype, progenies derived from mating between Tet1-KO males and wild-type females exhibit a number of variable phenotypes including placental, fetal and postnatal growth defects, and early embryonic lethality. These defects are, at least in part, caused by the dysregulation of imprinted genes, such as Peg10 and Peg3, which exhibit aberrant hypermethylation in the paternal allele of differential methylated regions (DMRs). RNA-seq reveals extensive dysregulation of imprinted genes in the next generation due to paternal functional loss of Tet1. Genome-wide DNA methylation analysis of E13.5 PGCs and sperm derived from Tet1-KO mice reveals hypermethylation of DMRs of imprinted genes in sperm, which can be traced back to PGCs. Dynamics of methylation change in Tet1-affected sites suggested that Tet1 swipes remaining methylation including imprinted genes at late reprogramming stage. We also revealed that Tet1play a role in paternal imprinting erasure in females germline. Thus, our study establishes a critical function for Tet1 in the erasure of genomic imprinting. Genome-wide DNA methylation analysis of E13.5 PGCs from control and Tet1-KO mice

2013-12-02 | E-GEOD-49762 | biostudies-arrayexpress

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