Nuclear IDH1 regulates human erythropoiesis by eliciting chromatin state reprogramming [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA925129 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23109656_1.fastq.gz | Fastqsanger.gz | |||
| SRR23109656_2.fastq.gz | Fastqsanger.gz | |||
| SRR23109657_1.fastq.gz | Fastqsanger.gz | |||
| SRR23109657_2.fastq.gz | Fastqsanger.gz | |||
| SRR23109658_1.fastq.gz | Fastqsanger.gz |
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Project description:Nuclear IDH1 regulates human erythropoiesis by eliciting chromatin state reprogramming
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Project description:Nuclear IDH1 regulates human erythropoiesis by eliciting chromatin state reprogramming
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Project description:Although, IDH1 has been recognized to play critical roles in the regulation of dynamic chromatin states, the mechanism remained largely unknown. Here, using the human erythropoiesis system, we presented an innovative perspective of metabolism independent role of nuclear IDH1. We discovered that IDH1 acted as a nuclear located chromatin-binding protein. Knockdown of IDH1 induced chromatin reorganization and subsequently aroused aberrant biological events germination on erythroid precursors in a metabolism independent manner. IDH1 knockdown induced genome-wide coordinate changes in the distribution and intensity of multiple histone marks, among which H3K79me3 was identified to be the decisive factor in chromatin state reprogramming. Integrating ChIP-seq, ATAC-seq and RNA-seq recognized SIRT1 to be the key gene affected by IDH1 deficiency. Taken together, these findings provided a novel insight for further clarifying the fundamental biological function of IDH1 which had substantial implications for an in-depth understanding of the pathogenesis of diseases with IDH1 dysfunction and accordingly the development of therapeutic strategies.
2025-01-01 | GSE222401 | GEO
Project description:Although, IDH1 has been recognized to play critical roles in the regulation of dynamic chromatin states, the mechanism remained largely unknown. Here, using the human erythropoiesis system, we presented an innovative perspective of metabolism independent role of nuclear IDH1. We discovered that IDH1 acted as a nuclear located chromatin-binding protein. Knockdown of IDH1 induced chromatin reorganization and subsequently aroused aberrant biological events germination on erythroid precursors in a metabolism independent manner. IDH1 knockdown induced genome-wide coordinate changes in the distribution and intensity of multiple histone marks, among which H3K79me3 was identified to be the decisive factor in chromatin state reprogramming. Integrating ChIP-seq, ATAC-seq and RNA-seq recognized SIRT1 to be the key gene affected by IDH1 deficiency. Taken together, these findings provided a novel insight for further clarifying the fundamental biological function of IDH1 which had substantial implications for an in-depth understanding of the pathogenesis of diseases with IDH1 dysfunction and accordingly the development of therapeutic strategies.
2025-01-01 | GSE222296 | GEO
Project description:Although, IDH1 has been recognized to play critical roles in the regulation of dynamic chromatin states, the mechanism remained largely unknown. Here, using the human erythropoiesis system, we presented an innovative perspective of metabolism independent role of nuclear IDH1. We discovered that IDH1 acted as a nuclear located chromatin-binding protein. Knockdown of IDH1 induced chromatin reorganization and subsequently aroused aberrant biological events germination on erythroid precursors in a metabolism independent manner. IDH1 knockdown induced genome-wide coordinate changes in the distribution and intensity of multiple histone marks, among which H3K79me3 was identified to be the decisive factor in chromatin state reprogramming. Integrating ChIP-seq, ATAC-seq and RNA-seq recognized SIRT1 to be the key gene affected by IDH1 deficiency. Taken together, these findings provided a novel insight for further clarifying the fundamental biological function of IDH1 which had substantial implications for an in-depth understanding of the pathogenesis of diseases with IDH1 dysfunction and accordingly the development of therapeutic strategies.
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Project description:Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations drive the development of gliomas and other human malignancies. Significant efforts are already underway to attempt to target mutant IDH in clinical trials. However, how mutation of IDH leads to tumorigenesis is poorly understood. Mutant IDH1 promotes epigenetic changes that promote tumorigenesis but the scale of these changes throughout the epigenome and the reversibility of these changes are unknown. Here, using both human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant IDH1-induced epigenomic reprogramming. We characterize the changes in the histone code landscape, DNA methylome, chromatin state, and transcriptional reprogramming that occur following IDH1 mutation and characterize the kinetics and reversibility of these alterations over time. We discover coordinate changes in the localization and intensity of multiple histone marks and chromatin states throughout the genome. These alterations result in systematic chromatin states changes, which result in widespread gene expression changes involving oncogenic pathways. Specifically, mutant IDH1 drives alterations in differentiation state and establishes a CD24+ population that features enhanced self-renewal and other stem-like properties. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented molecular portraits of mutant IDH1-dependent epigenomic reprogramming at high resolution. These findings have significant implications for our understanding the mechanisms underlying mutant IDH function and for optimizing therapeutic approaches to targeting IDH mutant tumors.
2017-08-23 | GSE85938 | GEO
Project description:Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations drive the development of gliomas and other human malignancies. Significant efforts are already underway to attempt to target mutant IDH in clinical trials. However, how mutation of IDH leads to tumorigenesis is poorly understood. Mutant IDH1 promotes epigenetic changes that promote tumorigenesis but the scale of these changes throughout the epigenome and the reversibility of these changes are unknown. Here, using both human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant IDH1-induced epigenomic reprogramming. We characterize the changes in the histone code landscape, DNA methylome, chromatin state, and transcriptional reprogramming that occur following IDH1 mutation and characterize the kinetics and reversibility of these alterations over time. We discover coordinate changes in the localization and intensity of multiple histone marks and chromatin states throughout the genome. These alterations result in systematic chromatin states changes, which result in widespread gene expression changes involving oncogenic pathways. Specifically, mutant IDH1 drives alterations in differentiation state and establishes a CD24+ population that features enhanced self-renewal and other stem-like properties. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented molecular portraits of mutant IDH1-dependent epigenomic reprogramming at high resolution. These findings have significant implications for our understanding the mechanisms underlying mutant IDH function and for optimizing therapeutic approaches to targeting IDH mutant tumors.
2017-08-23 | GSE85939 | GEO
Project description:Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations drive the development of gliomas and other human malignancies. Significant efforts are already underway to attempt to target mutant IDH in clinical trials. However, how mutation of IDH leads to tumorigenesis is poorly understood. Mutant IDH1 promotes epigenetic changes that promote tumorigenesis but the scale of these changes throughout the epigenome and the reversibility of these changes are unknown. Here, using both human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant IDH1-induced epigenomic reprogramming. We characterize the changes in the histone code landscape, DNA methylome, chromatin state, and transcriptional reprogramming that occur following IDH1 mutation and characterize the kinetics and reversibility of these alterations over time. We discover coordinate changes in the localization and intensity of multiple histone marks and chromatin states throughout the genome. These alterations result in systematic chromatin states changes, which result in widespread gene expression changes involving oncogenic pathways. Specifically, mutant IDH1 drives alterations in differentiation state and establishes a CD24+ population that features enhanced self-renewal and other stem-like properties. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented molecular portraits of mutant IDH1-dependent epigenomic reprogramming at high resolution. These findings have significant implications for our understanding the mechanisms underlying mutant IDH function and for optimizing therapeutic approaches to targeting IDH mutant tumors.
2017-08-23 | GSE85941 | GEO
Project description:Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations drive the development of gliomas and other human malignancies. Significant efforts are already underway to attempt to target mutant IDH in clinical trials. However, how mutation of IDH leads to tumorigenesis is poorly understood. Mutant IDH1 promotes epigenetic changes that promote tumorigenesis but the scale of these changes throughout the epigenome and the reversibility of these changes are unknown. Here, using both human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant IDH1-induced epigenomic reprogramming. We characterize the changes in the histone code landscape, DNA methylome, chromatin state, and transcriptional reprogramming that occur following IDH1 mutation and characterize the kinetics and reversibility of these alterations over time. We discover coordinate changes in the localization and intensity of multiple histone marks and chromatin states throughout the genome. These alterations result in systematic chromatin states changes, which result in widespread gene expression changes involving oncogenic pathways. Specifically, mutant IDH1 drives alterations in differentiation state and establishes a CD24+ population that features enhanced self-renewal and other stem-like properties. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented molecular portraits of mutant IDH1-dependent epigenomic reprogramming at high resolution. These findings have significant implications for our understanding the mechanisms underlying mutant IDH function and for optimizing therapeutic approaches to targeting IDH mutant tumors.
2017-08-23 | GSE85940 | GEO
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