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MacroH2A deletion causes neuronal developmental deficits and autism-like behavior in mice

ABSTRACT: Purpose:To further understand how MacroH2A regulates the proliferation of neural progenitor cells, RNA-seq was used to analyze genome-wide changes in the cerebral cortex and littermate wild type of E13.5 MacroH2A knockout mice Methods: Total RNA was extracted from wild-type E13.5 brain tissue and knock-out E13.5 brain tissue. Specifically, the Agilent 2100 Bioanalyzer was used for quality control and quantification. Total RNA was then converted to cDNA and combined with the library. Illumina HiSeq 2500 platform in Annoroad Genomics uses RNA sequencing analysis Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and knock-out mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected human MacroH2A plays a role in brain neuron development.

ORGANISM(S): Mus musculus

PROVIDER: GSE147064 | GEO | 2020/03/17

REPOSITORIES: GEO

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Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

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macroH2A histone variants act as a barrier upon reprogramming towards pluripotency

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Purification of macroH2A.1 and macroH2A.2 Nucleosomes from Fetal Mouse Liver

Project description:MacroH2As core histone variants have a unique structure that includes C-terminal nonhistone domain. MacroH2As are highly conserved in vertebrates, and are thought to regulate gene expression. However the nature of genes regulated by macroH2As and the biological significance of macroH2As for the organism remain unclear. Our gene expression studies indicate that macroH2A.1 and macroH2A.2 work together to regulate specific genes. In these studies we examine the distributions of macroH2A.1 and macroH2A.2 nucleosomes to determine if they are localized to the genes that show altered expression in macroH2A knockout mouse liver. MacroH2A.1 and macroH2A.2 nucleosomes prepared from ~ 50 fetal mouse livers were purified by thio-affinity chromatography. Five samples were sequenced: Thiopropyl Sepharose, Normal Liver - contains mononucleosomal DNA from macroH2A.1-containing nucleosomes; Activate Thiol Sepharose, Normal Liver - contains mononucleosomal DNA primarily from macroH2A.2-containing nucleosomes. Starting Material, Normal Liver - this is a reference samplefor the first two samples. It contains mononucleosomal DNA from bulk fetal liver chromatin. Activated Thiol Sepharose, Knockout Livers - this is a control sample that contains mononucleosomal DNA from non-macroH2A nucleosomes that contaminate the macroH2A.2 nucleosomes. This fraction was prepared from macroH2A1/2 double knockout fetal livers; Starting Material, Knockout Liver - this is a reference sample for the fourth sample. It contains mononucleosomal DNA from bulk chromatin prepared from macroH2A1/2 double knockout fetal livers.

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