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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants

ABSTRACT: Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants

PROVIDER: PRJNA685155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13242200_1.fastq.gz	Fastqsanger.gz
	SRR13242200_2.fastq.gz	Fastqsanger.gz
	SRR13253000_1.fastq.gz	Fastqsanger.gz
	SRR13253000_2.fastq.gz	Fastqsanger.gz
	SRR13242201_1.fastq.gz	Fastqsanger.gz

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [ChIP-Seq]

Project description:Point mutations within the histone H3.3 are frequent in aggressive childhood brain tumours known as paediatric high-grade gliomas (pHGGs). Intriguingly, different mutations arise in discrete anatomical regions: H3.3-G34R within the forebrain and H3.3-K27M preferentially within the hindbrain. The reasons for this contrasting aetiology are unknown. By engineering human foetal neural stem cell cultures from distinct regions, we demonstrate here that cell-intrinsic regional identity provides differential responsiveness to each mutant that mirrors the origins of pHGGs. Focusing on H3.3-G34R, we find that the oncohistone supports proliferation of forebrain cells, while inducing a cytostatic response in the hindbrain. Mechanistically, H3.3-G34R does not impose widespread transcriptional or epigenetic changes, but impairs recruitment of ZMYND11, a transcriptional repressor of highly expressed genes. We therefore propose that H3.3-G34R promotes tumorigenesis by stabilising the expression of key progenitor genes and, thus, locking initiating forebrain cells into their preexisting immature state.

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [RNA-Seq]

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [ChIP-Seq]

Project description:Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [ChIP-Seq]

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Project description:Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants [RNA-Seq]

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants.

Project description:Point mutations within the histone H3.3 are frequent in aggressive childhood brain tumors known as pediatric high-grade gliomas (pHGGs). Intriguingly, distinct mutations arise in discrete anatomical regions: H3.3-G34R within the forebrain and H3.3-K27M preferentially within the hindbrain. The reasons for this contrasting etiology are unknown. By engineering human fetal neural stem cell cultures from distinct brain regions, we demonstrate here that cell-intrinsic regional identity provides differential responsiveness to each mutant that mirrors the origins of pHGGs. Focusing on H3.3-G34R, we find that the oncohistone supports proliferation of forebrain cells while inducing a cytostatic response in the hindbrain. Mechanistically, H3.3-G34R does not impose widespread transcriptional or epigenetic changes but instead impairs recruitment of ZMYND11, a transcriptional repressor of highly expressed genes. We therefore propose that H3.3-G34R promotes tumorigenesis by focally stabilizing the expression of key progenitor genes, thereby locking initiating forebrain cells into their pre-existing immature state.

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Regional identity of human neural stem cells determinesoncogenic responses to histone 1H3.3 mutants

Project description:Regional identity of human neural stem cells determinesoncogenic responses to histone 1H3.3 mutants

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Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants

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

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SOX1 Determines the Regional Identity of Neural Progenitors Differentiated from Human Embryonic Stem Cells

Project description:SOX1 Determines the Regional Identity of Neural Progenitors Differentiated from Human Embryonic Stem Cells

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SOX1 Determines the Regional Identity of Neural Progenitors Differentiated from Human Embryonic Stem Cells

Project description:During human embryogenesis, primitive neural cells start to be generated at the time of gastrulation and gradually acquire regional identities, which is a process called neural patterning. But how intrinsic factors respond to exogenous patterning signals remains poorly understood. Human Embryonic Stem Cells (hESCs) provide a great model to recapitulate this process. Through exogenous manipulation of canonical WNT signaling activation during neural differentiation, dose-dependent specification of regionally defined neural progenitors ranging from the telencephalic forebrain to posterior hindbrain could be rapidly and efficiently induced. Unexpectedly, we find that SOX1, generally referred as a pan-neural gene, displays a regional specific distribution in the human neural patterning process. To investigate the expression and function of SOX1 efficiently, we have generated the SOX1-EGFP reporter and SOX1-knockout (KO) hESC lines using the CRISPR/Cas9 system. SOX1 is initially expressed across the mes–met border and peaked in the metencephalon region at the early regional specification stage. Its depletion leads to the posterior shift of the mes–met border. Therefore, SOX1 is required to define the border at a correct region. In-depth analysis of SOX1 ChIP-sequencing and transcriptome data will provide more insights into how SOX1 determines the mes-met border formation and identify the downstream targets of SOX1. This study identifies SOX1 as one of the intrinsic factors key for the prepattern establishment in the developing central nervous system, particularly for defining the isthmus position.

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Tbr1 regulates regional and laminar identity of postmitotic neurons in developing neocortex

Project description:Areas and layers of the cerebral cortex are specified by genetic programs that are initiated in progenitor cells and then, implemented in postmitotic neurons. Here, we report that Tbr1, a transcription factor expressed in postmitotic projection neurons, exerts positive and negative control over both regional (areal) and laminar identity. Tbr1 null mice exhibited profound defects of frontal cortex and layer 6 differentiation, as indicated by down-regulation of gene-expression markers such as Bcl6 and Cdh9. Conversely, genes that implement caudal cortex and layer 5 identity, such as Bhlhb5 and Fezf2, were up-regulated in Tbr1 mutants. Tbr1 implements frontal identity in part by direct promoter binding and activation of Auts2, a frontal cortex gene implicated in autism. Tbr1 regulates laminar identity in part by downstream activation or maintenance of Sox5, an important transcription factor controlling neuronal migration and corticofugal axon projections. Similar to Sox5 mutants, Tbr1 mutants exhibit ectopic axon projections to the hypothalamus and cerebral peduncle. Together, our findings show that Tbr1 coordinately regulates regional and laminar identity of postmitotic cortical neurons. Mouse E14.5 neocortices and Postnatal day (P) 0.5 brains: E14.5 neocortices KO, 3; E14.5 neocortices WT, 3; Postnatal day (P) 0.5 brains frontal WT, 4; Postnatal day (P) 0.5 brains frontal KO, 4; Postnatal day (P) 0.5 brains parietal WT, 4; Postnatal day (P) 0.5 brains parietal KO, 4; Postnatal day (P) 0.5 brains occipital WT, 4; Postnatal day (P) 0.5 brains occipital KO, 4.

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