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Mina53 regulates the neural stem cell pool by acting as an argnine demethlysae

ABSTRACT: Mina53 regulates the neural stem cell pool by acting as an argnine demethlysae

PROVIDER: PRJNA974040 | ENA |

REPOSITORIES: ENA

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Mina53 regulates the neural stem cell pool by acting as an arginine demethylase

Project description:Mina53 regulates the neural stem cell pool by acting as an arginine demethylase

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Mina53 regulates the neural stem cell pool by acting as an argnine demethlysae

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Mina53 regulates the neural stem cell pool by acting as an arginine demethylase

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Mina53 demethylates histone 4 arginine 3 asymmetric di-methylation to regulate neural stem/progenitor cell identity

Project description:Arginine methylation of histones plays a critical role in regulating gene expression. The writers (methyltransferases) and readers of methylarginine marks are well-known, but the erasers－arginine demethylases－remain mysterious. Here we identify Myc-induced nuclear antigen 53 (Mina53), a jumonji C domain containing protein, as an arginine demethylase for removing asymmetric di-methylation at arginine 3 of histone H4 (H4R3me2a). Using photoaffinity capture method, we first identified Mina53 as an interactor of H4R3me2a. Biochemical assays in vitro and in cells characterized the arginine demethylation activity of Mina53. Molecular dynamics simulations provide further atomic-level evidence that Mina53 acts on H4R3me2a. In a transgenic mouse model, specific Mina53 deletion in neural stem/progenitor cells prevented H4R3me2a demethylation at distinct genes clusters, dysregulating genes important for neural stem/progenitor cell proliferation and differentiation, and consequently impairing the cognitive function of mice. Collectively, we identify Mina53 as a bona fide H4R3me2a eraser, expanding the understanding of epigenetic gene regulation.

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Genes regulated by Mina53 in Mina53-KO NSPCs compared with wild-type NSPCs.

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Sequentially acting Sox transcription factors in neural lineage development

Project description:This SuperSeries is composed of the following subset Series: GSE33059: Sequentially acting Sox transcription factors in neural lineage development [ChIP-seq] GSE33060: Sequentially acting Sox transcription factors in neural lineage development [RNA-seq] GSE33061: Sequentially acting Sox transcription factors in neural lineage development [microarray] Refer to individual Series

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Genes enriched with H4R3me2a modification in Mina53-KO NSPCs compared with wild-type NSPCs.

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Genes regulated by Mina53 in Mina53-KO NSPCs compared with wild-type NSPCs.

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A lysine demethylase-independent function of Phf2 regulates cohesin-mediated DNA replication for neural stem cell activation

Project description:The activation of quiescent neural stem cells (qNSCs) in the dentate gyrus is required for lifelong neurogenesis. However, the mechanisms that promote the exit of neural stem cells (NSCs) from quiescence remain elusive. We demonstrate that the expression of plant homeodomain finger protein 2 (Phf2) activates the exit of postnatal mouse NSC from shallow quiescence. Loss of Phf2 prevents NSC activation and neurogenesis in postnatal 30 (P30) mice but does not decrease the label-retaining NSC pool, indicating that Phf2 is not required for the exit of NSC from quiescence. NSC-specific deletion of Phf2 modestly compromises embryonic mouse NSC proliferation without increasing apoptosis, indicating that Phf2 is crucial for embryonic development. Moreover, human cortical organoids reveal that Phf2 promotes NPC proliferation via a lysine demethylase-independent manner. Mechanistically, Phf2 directly binds to the cohesion complex via Rad21 and regulates the DNA replication in mouse NSC by associating with the cohesion complex releasing protein Wapl activity. Our study identifies the Phf2-cohesin complex mediated DNA replication for neural stem cell activation in a lysine demethylase-independent manner.

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