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Mus musculus

ABSTRACT: The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [RNA-Seq]

PROVIDER: PRJNA376129 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5274800_1.fastq.gz	Fastqsanger.gz
	SRR5274800_2.fastq.gz	Fastqsanger.gz
	SRR5274797_1.fastq.gz	Fastqsanger.gz
	SRR5274797_2.fastq.gz	Fastqsanger.gz
	SRR5274798_1.fastq.gz	Fastqsanger.gz

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The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture

Project description:The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture

| PRJNA376123 | ENA

Mus musculus

Project description:The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [Hi-C]

| PRJNA376128 | ENA

Mus musculus

Project description:The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 1]

| PRJNA376127 | ENA

The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 2]

Project description:The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 2]

| PRJNA408237 | ENA

The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 2]

Project description:Here we show that HNRNPU, the major nuclear matrix attachment factor, is necessary to maintain proper nuclear architecture in mouse hepatocytes. Upon HNRNPU depletion, the interactions between chromatin and nuclear lamina have been changed dramatically；chromatin organization is globally changed; boundaries of topologically associating domains (TADs) become weaker; inter-TAD interactions are increased; thousands of genes are significantly altered coincident with 3D chromatin changes. Mechanically, HNRNPU interacts with CTCF and RAD21, which affects the binding of RAD21 to the chromatin significantly, whereas CTCF bindings are almost unchanged, what’ more, the decrease of binding strengths are highly correlated with the weakness of loop bounded by Rad21. Taken together, we identify HNRNPU as a key regulator of chromatin architecture, and our data suggest the importance of nuclear matrix associating factors in 3D genome organization.

2017-12-03 | GSE104098 | GEO

The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [ChIP-Seq 1]

Project description:Higher-order chromatin conformation plays critical role in regulating gene expression and biological development, here we show that HNRNPU, a nuclear matrix attachment factor, is a regulator of 3D genome architecture at multiple levels in mouse hepatocytes. We demonstrate that depletion of HNRNPU results into a global reorganization of nuclear bodies and re-localization of chromatin towards nuclear periphery. Additionally, upon HNRNPU depletion, chromatin interactions between A-type (active) and B-type (inactive) compartments increase significantly but those among same types of compartments decrease significantly, which associate with global gene expression changes. While TADs remain largely invariant, both inter- and intra-TAD interactions increase significantly in A-type compartments but decrease in B-type compartments. Mechanically, HNRNPU complexes with structural proteins CTCF and RAD21; depletion of HNRNPU specifically weakens the bindings of RAD21 to the chromatin, which is highly correlated with the weakness of chromatin loops.

2017-12-03 | GSE95113 | GEO

The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [Hi-C]

2017-12-03 | GSE95112 | GEO

The nuclear matrix associating protein HNRNPU functions as a key regulator of 3D genome architecture [RNA-Seq]

2017-12-03 | GSE95111 | GEO

Genome-wide maps of nuclear lamina interactions in AML12 cells upon HNRNPU KD [DamID]

2017-12-03 | GSE95115 | GEO

Chromatin architecture as a checkpoint for NASH-associated liver injury

Project description:Nonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress-induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. Here we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA-seq and ChIP-seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte-specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated the molecular signature of NASH and sensitized mice to diet-induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB that promotes inflammatory signaling in hepatocytes and stress-induced cell death. These findings illustrate a novel mechanism through which disruptions of chromatin architecture drive the emergence of disease-specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.

2019-09-10 | GSE131336 | GEO

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