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Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription

ABSTRACT: Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription

PROVIDER: PRJNA267638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1654840.fastq.gz	Fastqsanger.gz
	SRR1656790.fastq.gz	Fastqsanger.gz
	SRR1654841.fastq.gz	Fastqsanger.gz
	SRR1656791.fastq.gz	Fastqsanger.gz
	SRR1654842.fastq.gz	Fastqsanger.gz

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Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription [ChIP-Seq]

Project description:The application of massively-parallel sequencing (MPS) technology to understanding how the genome is regulated is of major importance, as we now appreciate sequence variants associated with common heritable diseases to be enriched at regulatory elements in the genome. There is, however, an enormous challenge inherent to these studies, which are much more varied as assays and in terms of analytical approaches than the approaches used to define the sequence variants themselves. For example, there are a plethora of assays that test 5-methylcytosine genome-wide, numerous different analytical approaches to defineing peaks from chromatin immunoprecipitation sequencing (ChIP-seq), and increasingly diverse aspects of genomic regulation being studied. The extremely large data sets generated do not lend themselves to distribution without some degree of pre-processing, and the hardware requirements for running these analyses are often substantial. We have highlighted these concerns previously, but the central concern for our field is that genomics research is especially prone to poor reproducibility, and is a prime candidate for implementation of measures that could help to address this general problem. To illustrate the practical issues involved in genomics reproducibility, we sought to analyze our data and data from three previoulsy published studies of the histone demethylase KDM5B using the same analytical approaches. In particular we compared the results of our ChIP-seq experiments to previous H3K4me3 and Kdm5b ChIP-seq data in the public database: GSE31966 and GSE53087 (only samples GSM1282126, GSM1282127, GSM1282129, GSM1282131, and GSM1282132). Re-analyzed (ChIP-seq) data from GSE31966 and GSE53087 are linked below as supplementary files.

2020-03-21 | GSE63286 | GEO

Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription [HELP-tagging]

Project description:The application of massively-parallel sequencing (MPS) technology to understanding how the genome is regulated is of major importance, as we now appreciate sequence variants associated with common heritable diseases to be enriched at regulatory elements in the genome. There is, however, an enormous challenge inherent to these studies, which are much more varied as assays and in terms of analytical approaches than the approaches used to define the sequence variants themselves. For example, there areis a plethora of assays that test 5-methylcytosine genome-wide, numerous different analytical approaches to defineing peaks from chromatin immunoprecipitation sequencing (ChIP-seq), and increasingly diverse aspects of genomic regulation being studied. The extremely large data sets generated do not lend themselves to distribution without some degree of pre-processing, and the hardware requirements for running these analyses are often substantial. We have highlighted these concerns previously, but the central concern for our field is that genomics research is especially prone to poor reproducibility, and is a prime candidate for implementation of measures that could help to address this general problem.To illustrate the practical issues involved in genomics reproducibility, we sought to analyze our and three previoulsy published studies of the histone demethylase KDM5B using the same analytical approaches.

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Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription [RNA-Seq]

Project description:The application of massively-parallel sequencing (MPS) technology to understanding how the genome is regulated is of major importance, as we now appreciate sequence variants associated with common heritable diseases to be enriched at regulatory elements in the genome. There is, however, an enormous challenge inherent to these studies, which are much more varied as assays and in terms of analytical approaches than the approaches used to define the sequence variants themselves. For example, there areis a plethora of assays that test 5-methylcytosine genome-wide, numerous different analytical approaches to defineing peaks from chromatin immunoprecipitation sequencing (ChIP-seq), and increasingly diverse aspects of genomic regulation being studied. The extremely large data sets generated do not lend themselves to distribution without some degree of pre-processing, and the hardware requirements for running these analyses are often substantial. We have highlighted these concerns previously, but the central concern for our field is that genomics research is especially prone to poor reproducibility, and is a prime candidate for implementation of measures that could help to address this general problem.To illustrate the practical issues involved in genomics reproducibility, we sought to analyze our and three previoulsy published studies of the histone demethylase KDM5B using the same analytical approaches.

2020-03-21 | GSE63285 | GEO

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Project description:The evolutionary impact of Intragenic FliA Promoters

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The evolutionary impact of Intragenic FliA Promoters

Project description:The evolutionary impact of Intragenic FliA Promoters

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Project description:Transcription-driven Chromatin Repression of Intragenic Promoters

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Transcription-driven Chromatin Repression of Intragenic Promoters

Project description:The goal of this study is to investigate a chromatin-based mechanism that suppresses intragenic initiation of RNAPII transcription in A.thaliana. We demonstrate that RNAPII transcription across gene promoters represses their function in plants. The FACT histone chaperone complex is required for this repression mechanism by co-transcriptionally enforcing elevated levels of H3K4me1 at repressed intragenic promoters;

2018-04-26 | GSE113677 | GEO

KDM5B focuses H3K4 methylation near promoters and enhancers during embryonic stem cell self-renewal and differentiation [ChIP-Seq]

Project description:Pluripotency of embryonic stem (ES) cells is controlled in part by chromatin-modifying factors that regulate histone H3 lysine 4 (H3K4) methylation. However, it remains unclear how H3K4 demethylation contributes to ES cell function. Here, we show that KDM5B, which demethylates lysine 4 of histone H3, co-localizes with H3K4me3 near promoters and enhancers of active genes in ES cells; its depletion leads to spreading of H3K4 methylation into gene bodies and enhancer shores, indicating that KDM5B functions to focus H3K4 methylation at promoters and enhancers. Spreading of H3K4 methylation to gene bodies and enhancer shores is linked to defects in gene expression programs and enhancer activity, respectively, during self-renewal and differentiation of KDM5B-depleted ES cells. KDM5B critically regulates H3K4 methylation at bivalent genes during differentiation in the absence of LIF or Oct4. We also show that KDM5B and LSD1, another H3K4 demethylase, co-regulate H3K4 methylation at active promoters but they retain distinct roles in demethylating gene body regions and bivalent genes. Our results provide global and functional insight into the role of KDM5B in regulating H3K4 methylation marks near promoters, gene bodies, and enhancers in ES cells and during differentiation. ChIP-Seq for KDM5B, H3K4 methylation and H3K27ac in murine shLuc, shKdm5b, shLuc-LSD1i, shKdm5b-LSD1i ES cells, and during differentiation of shLuc and shKdm5b ES cells for 2 days, 3 days, and 4 days without LIF.

2014-01-27 | E-GEOD-53087 | biostudies-arrayexpress

KDM5B focuses H3K4 methylation near promoters and enhancers during embryonic stem cell self-renewal and differentiation [RNA-Seq]

Project description:Pluripotency of embryonic stem (ES) cells is controlled in part by chromatin-modifying factors that regulate histone H3 lysine 4 (H3K4) methylation. However, it remains unclear how H3K4 demethylation contributes to ES cell function. Here, we show that KDM5B, which demethylates lysine 4 of histone H3, co-localizes with H3K4me3 near promoters and enhancers of active genes in ES cells; its depletion leads to spreading of H3K4 methylation into gene bodies and enhancer shores, indicating that KDM5B functions to focus H3K4 methylation at promoters and enhancers. Spreading of H3K4 methylation to gene bodies and enhancer shores is linked to defects in gene expression programs and enhancer activity, respectively, during self-renewal and differentiation of KDM5B-depleted ES cells. KDM5B critically regulates H3K4 methylation at bivalent genes during differentiation in the absence of LIF or Oct4. We also show that KDM5B and LSD1, another H3K4 demethylase, co-regulate H3K4 methylation at active promoters but they retain distinct roles in demethylating gene body regions and bivalent genes. Our results provide global and functional insight into the role of KDM5B in regulating H3K4 methylation marks near promoters, gene bodies, and enhancers in ES cells and during differentiation. RNA-Seq of murine shLuc and shKdm5b ES cells differentiated for 72h in the absence of LIF.

2014-01-27 | E-GEOD-53090 | biostudies-arrayexpress

Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-21 | GSE63287 | GEO