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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [CD90.2+ T cells, RNA-seq]

ABSTRACT: Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [CD90.2+ T cells, RNA-seq]

PROVIDER: PRJNA1095974 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28549335_1.fastq.gz	Fastqsanger.gz
	SRR28549335_2.fastq.gz	Fastqsanger.gz
	SRR28549336_1.fastq.gz	Fastqsanger.gz
	SRR28549336_2.fastq.gz	Fastqsanger.gz
	SRR28549337_1.fastq.gz	Fastqsanger.gz

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice

Project description:Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [NeuN+ hippocampal neurons]

Project description:Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [NeuN+ hippocampal neurons]

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [CD90.2+ T cells]

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [NeuN+ hippocampal neurons]

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [NeuN+ hippocampal neurons]

Project description:Many Mendelian developmental disorders caused by coding variants in epigenetic regulators have now been discovered. Epigenetic regulators are broadly expressed, and each of these disorders typically exhibits phenotypic manifestations from many different organ systems. An open question is whether the chromatin disruption -- the root of the pathogenesis -- is similar in the different disease-relevant cell types. This is possible in principle, since all these cell-types are subject to effects from the same causative gene, that has the same kind of function (e.g. methylates histones) and is disrupted by the same germline variant. We focus on mouse models for Kabuki syndrome types 1 and 2, and find that the chromatin accessibility abnormalities in neurons are mostly distinct from those in B or T cells. This is not because the neuronal abnormalities occur at regulatory elements that are only active in neurons. Neurons, but not B or T cells, show preferential chromatin disruption at CpG islands and at regulatory elements linked to aging. A sensitive analysis reveals that the regions disrupted in B/T cells do exhibit chromatin accessibility changes in neurons, but these are very subtle and of uncertain functional significance. Finally, we identify a small set of regulatory elements disrupted in all three cell types. Our findings reveal the cellular-context-specific effect of variants in epigenetic regulators, and suggest that blood-derived episignatures may not be well-suited for understanding the mechanistic basis of neurodevelopment in Mendelian disorders of the epigenetic machinery.

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Neuron-specific chromatin disruption at CpG islands and aging-related regions in Kabuki syndrome mice [NeuN+ hippocampal neurons]

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CpG islands shape the epigenome landscape.

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KDM2B binds CpG islands and modulates recruitment of Ring1b

Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs.

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