The Heterogeneous Nuclear Ribonucleoprotein U (HNRNPU) is the Safeguard of Neural Stem Cell Viability
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ABSTRACT:
PROVIDER: PRJNA752358 | ENA |
REPOSITORIES: ENA
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Project description:Genetic variants affecting Heterogeneous Nuclear Ribonucleoprotein U (HNRNPU) have been identified in several neurodevelopmental disorders (NDDs). HNRNPU is widely expressed in the human brain and shows the highest postnatal expression in the cerebellum. Recent studies have investigated the role of HNRNPU in cerebral cortical development, but the effects of HNRNPU deficiency on cerebellar development remain unknown. Here, we describe the molecular and cellular outcomes of HNRNPU locus deficiency during in vitro neural differentiation of patient-derived and isogenic neuroepithelial stem cells with a hindbrain profile. We demonstrate that HNRNPU deficiency leads to chromatin remodeling of A/B compartments, and transcriptional rewiring, partly by impacting exon inclusion during mRNA processing. Genomic regions affected by the chromatin restructuring and host genes of exon usage differences show a strong enrichment for genes implicated in epilepsies, intellectual disability, and autism. Lastly, we show that at the cellular level. HNRNPU downregulation leads to altered neurogenesis and an increased fraction of neural progenitors in the maturing neuronal population. We conclude that, HNRNPU locus is involved in delayed commitment of neural progenitors to neuronal maturation in cell types with hindbrain profile.
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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.
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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.
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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.
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