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The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE255862 | GEO | 2024/11/29

REPOSITORIES: GEO

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The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [RNA-seq]

Project description:Induced pluripotent stem cells (iPSCs) technology offers great promise for scientific research and clinical applications. iPSCs can be generated from various cell types through different strategies. Two different pluripotent states, naive and primed, can be captured in vitro, corresponding to the pre- and post-implantation stages of in vivo development, respectively, with naive pluripotency being considered to possess better developmental potential. We can obtain naïve iPSCs and primed iPSCs through somatic cell reprogramming. Despite well-characterized transcriptional and epigenetic changes, the dynamic of the chromatin landscape during naïve and primed iPSC reprogramming is poorly understood, especially in humans. In this study, we applied ATAC-seq and RNA-seq to delineate the chromatin landscape in the human secondary reprogramming system towards naive and primed pluripotency. We identified several transcription factors and epigenetic factors which were crucial to reprogramming chromatin remodeling. We found that two isoforms of the same gene PRDM1, PRDM1alpha and PRDM1beta, targeted different genomic loci to function in divergent roles during naive reprogramming. We proposed a cross-regulation model of PRDM1alpha and PRDM1beta function. Together, this research highlights the diversity of the transcription factors in determining the chromatin landscape dynamics and regulating pluripotent cell fates.

2024-11-29 | GSE255861 | GEO

The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [CUT&Tag]

2024-11-29 | GSE255860 | GEO

The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [ATAC-seq]

Project description:Induced pluripotent stem cells (iPSCs) technology offers great promise for scientific research and clinical applications. iPSCs can be generated from various cell types through different strategies. Two different pluripotent states, naive and primed, can be captured in vitro, corresponding to the pre- and post-implantation stages of in vivo development, respectively, with naive pluripotency being considered to possess better developmental potential. We can obtain naïve iPSCs and primed iPSCs through somatic cell reprogramming. Despite well-characterized transcriptional and epigenetic changes, the dynamic of the chromatin landscape during naïve and primed iPSC reprogramming is poorly understood, especially in humans. In this study, we applied ATAC-seq and RNA-seq to delineate the chromatin landscape in the human secondary reprogramming system towards naive and primed pluripotency. We identified several transcription factors and epigenetic factors which were crucial to reprogramming chromatin remodeling. We found that two isoforms of the same gene PRDM1, PRDM1α and PRDM1β, targeted different genomic loci to function in divergent roles during naive reprogramming. We proposed a cross-regulation model of PRDM1α and PRDM1β function. Together, this research highlights the diversity of the transcription factors in determining the chromatin landscape dynamics and regulating pluripotent cell fates.

2024-11-29 | GSE255859 | GEO

The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming

Project description:The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming

| PRJNA1076848 | ENA

The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [CUT&Tag]

Project description:The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [CUT&Tag]

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The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [RNA-seq]

Project description:The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [RNA-seq]

| PRJNA1077079 | ENA

The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [ATAC-seq]

Project description:The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [ATAC-seq]

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Critical role of transient activation of human endogenous retroviruses during reprogramming toward pluripotency

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-04 | E-GEOD-56569 | biostudies-arrayexpress

Two factor reprogramming of human neural stem cells into pluripotency.

Project description:BackgroundReprogramming human somatic cells to pluripotency represents a valuable resource for the development of in vitro based models for human disease and holds tremendous potential for deriving patient-specific pluripotent stem cells. Recently, mouse neural stem cells (NSCs) have been shown capable of reprogramming into a pluripotent state by forced expression of Oct3/4 and Klf4; however it has been unknown whether this same strategy could apply to human NSCs, which would result in more relevant pluripotent stem cells for modeling human disease.Methodology and principal findingsHere, we show that OCT3/4 and KLF4 are indeed sufficient to induce pluripotency from human NSCs within a two week time frame and are molecularly indistinguishable from human ES cells. Furthermore, human NSC-derived pluripotent stem cells can differentiate into all three germ lineages both in vitro and in vivo.Conclusions/significanceWe propose that human NSCs represent an attractive source of cells for producing human iPS cells since they only require two factors, obviating the need for c-MYC, for induction into pluripotency. Thus, in vitro human disease models could be generated from iPS cells derived from human NSCs.

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Integrative analysis of reprogramming human fibroblast cells to naïve pluripotency

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

2018-03-03 | GSE89072 | GEO