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Mina53 regulates the expression of downstream genes in NSPC cells by its arginine demethylase activity on H4R3me2a

ABSTRACT: Mina53 regulates the expression of downstream genes in NSPC cells by its arginine demethylase activity on H4R3me2a

PROVIDER: PRJNA1150155 | ENA |

REPOSITORIES: ENA

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Mina53 regulates the expression of downstream genes in NSPC cells by its arginine demethylase activity on H4R3me2a

Project description:In order to investigate the role of Mina53 in the NSPC proliferation and differentiation, we performed RNA-seq using Mina53-KO NSPCs and wild-type NSPCs; we performed CUT-TAG using anti-H4R3me2a antibody in Mina53-KO NSPCs and wild-type NSPCs.

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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.

2024-10-22 | PXD045247 | Pride

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

Project description:To investigate the function Mina53 in the regulation of neural stem cells proliferation and differentiation, we collect neural stem cells which Mina53 has been knocked down by shRNA.

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

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

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Histone arginine demethylation by RDMe1

Project description:Histone methylation mainly occurs on lysine and arginine residues. While lysine methylation can be removed by LSD1 and JmjC domain-containing demethylases, the existence of histone arginine demethylases is highly controversial. Here, we performed a high-content cell-based screening of a cDNA library containing 2,500 nuclear proteins and identified RDMe1 as a histone arginine demethylase. Overexpression of RDMe1 in HEK293T cells reduces H3R2me1/2a and H4R3me1/2a levels. In vitro, RDMe1 specifically demethylates H3R2me1/2a and H4R3me1/2a, and generates formaldehyde and succinate. The enzymatic activity requires Fe(II) and α-ketoglutarate as cofactors. RDMe1 is mainly located in the nucleolar and regulates rRNA transcription by demethylating H3R2me2a. ChIP-seq reveals that RDMe1 demethylates H4R3me2a in the promoter in a genome-wide scale. NMR reveals that RDMe1 binds iron and substrate peptides with N and C termini, respectively. Mutation of the iron binding residues abolished the binding and the demethylase activity. Thus, we identify a histone arginine demethylase and reveal the reversibility of arginine methylation.

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