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Expression data from liver samples overxpressing either the GFP or Phf2

ABSTRACT: The GFP or Phf2 were overexpressed in the liver of C57Bl6/J mice through adenoviral gene delivery. Mice were studied in the fed state 3 weeks later. We used microarray analysis to detail the global programme of gene expression underlying Phf2 overexpression and identified distinct classes of up and down regulated genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE61575 | GEO | 2015/10/01

SECONDARY ACCESSION(S): PRJNA261519

REPOSITORIES: GEO

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Expression data from liver samples overxpressing either the GFP or ChREBP

Project description:The GFP or ChREBP were overexpressed in the liver of C57Bl6/J mice through adenoviral gene delivery. Mice were studied in the fed state 3 weeks later. We used microarray analysis to detail the global programme of gene expression underlying ChREBP overexpression and identified distinct classes of up and down regulated genes.

2015-10-01 | GSE61576 | GEO

Expression data from liver samples overexpressing either GFP or ChREBP

Project description:The GFP or ChREBP were overexpressed in the liver of C57Bl6/J mice through adenoviral gene delivery. Mice were studied in the fed state 3 weeks later. We used microarray analysis to detail the global program of gene expression underlying ChREBP overexpression and identified distinct classes of up and down regulated genes.

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QuantSeq analysis in the hippocampus of WT and PHF2 t/g mice

Project description:Long-term memory formation is attributed to experience-dependent gene expression. Dynamic changes in histone methylation status are essential for epigenetic regulation of memory consolidation-related genes. Here, we demonstrated that plant homeodomain finger protein 2 (PHF2) histone demethylase is upregulated in the mouse hippocampus during experience and plays an essential role in memory formation. QuantSeq analysis was performed to examine differential gene expression in the hippocampus of WT and PHF2 t/g mice. Transgenic mice were created by injecting the CMV-Flag-PHF2 vector into fertilized eggs from C57BL6 mice. Transgenic lines were established from 9 founders that were identified via PCR-based genotyping. Among the transgenic lines, mice with high PHF2 expressed brains were singled out for breeding. First, selected heterozygote males were bred with heterozygote females which produced homozygote, heterozygote and wild littermates. Since it is difficult to differentiate between hetero and homo mice with genotyping, we separated homo mice from hetero mice by breeding each of hetero and homo mice with wild type mice and confirming the genotypes of their offspring. In other words, hetero mice bred with wild type mice would have both wild type and hetero genotype of offspring, while homo mice bred with wild type mice would only have hetero genotype of offspring. Through this process, we particularly selected the homo mice and this transgenic line was used and maintained for this experiment.

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ChIP-seq experiment of PHF2 and H3K9me2 in NSCs

Project description:Histone H3 lysine 9 methylation (H3K9me) is essential for cellular homeostasis; however, its contribution to development is not well established. Here, we demonstrate that the H3K9me2 demethylase PHF2 is essential for neural progenitor proliferation in vitro and for early neurogenesis in the chicken spinal cord. Using genome-wide analyses and biochemical assays we show that PHF2 controls the expression of critical cell cycle progression genes, particularly those related to DNA replication, by keeping low levels of H3K9me3 at promoters. Accordingly, PHF2 depletion induces R-loop accumulation that leads to extensive DNA damage and cell cycle arrest. These data reveal a role of PHF2 as a guarantor of genome stability that allows proper expansion of neural progenitors during development.

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Hi-C in neural stem cells before and after Phf2 KO

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Interactome analysis of PHF2 using LC-MS combined with an immunoprecipitation assay

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2023-10-18 | PXD044277 | Pride

PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity (ChIP-Seq)

Project description:Heterochromatin stability is crucial for progenitor proliferation during development. It relays on the maintenance of local hubs of H3K9me. However, the mechanisms underlying the establishment of competent local levels of H3K9me remain poorly understood. To address this intriguing question, we used a neural stem cell (NSC) model to analyze the significance of the H3K9me2 demethylase PHF2, which is crucial for progenitor proliferation. Through mass spectroscopy and genome-wide assays, we uncovered that PHF2 interacts with heterochromatin components and it is enriched at pericentromeric heterochromatin (PcH) boundaries. This binding is essential for maintaining silenced the satellite repeats and to prevent DNA damage and genome instability. To do that, PHF2 balances H3K9me3 levels at these boundaries to ensure high H3K9me3 levels at satellite repeats. Mechanistically, we discover that while its catalytic and PHD domains are indispensable, the intrinsically disordered region within PHF2 is dispensable for stabilizing PcH. Altogether, our study sheds light on the intricate relationship between heterochromatin stability and progenitor proliferation during mammalian neurogenesis.

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PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity (ATAC-Seq)

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Rna-seq profiling of epigenetic regulator Phf2 in neural stem cells

Project description:Important hallmark of neurogenesis is activation of quiescent neural stem cells (NSC) in dentate gyrus. Precise mechanisms of NSC activation are not fully clear. In the current study we interrogate the role of homeodomain finger protein 2 (Phf2) in this process. Here we performed mouse transcriptome RNA-seq profiling of epigenetic regulator Phf2 in neural stem cells without and with knock-down in order to uncover mechanistic components/pathways affecting protein translational capacity in activated NSC.

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