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Effect of a myofiber-specific HIRA conditional knockout on gene expression in mouse skeletal muscle at 6 months of age

ABSTRACT: We performed gene expression profiling by microarray using RNA extracted from the tibialis anterior of control and Hira myofiber-specific conditional knockout mice at 6 months of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed loci. Conditional knockout of Hira in myofibers improved strength and endurance, caused hypertrophy and regeneration, and increased the percentage of type I fibers. These results illustrate the physiological consequences of disrupting Hira-mediated chromatin assembly in myofibers.

ORGANISM(S): Mus musculus

PROVIDER: GSE90900 | GEO | 2017/06/26

SECONDARY ACCESSION(S): PRJNA356295

REPOSITORIES: GEO

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Effect of HIRA deletion on gene expression in mouse skeletal muscle at 6 weeks of age

Project description:We performed gene expression profiling by microarray using RNA extracted from the tibialis anterior of control and Hira myofiber-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed loci. Conditional knockout of Hira in myofibers caused hypertrophy, degeneration, and increased the percentage of type I fibers. These results illustrate the physiological consequences of disrupting Hira-mediated chromatin assembly in myofibers.

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Chromatin assembly factor HIRA is essential for the maintenance of hematopoiesis

Project description:HIRA is a histone chaperone that deposits the histone variant H3.3 in transcriptionally active genes. HIRA is essential for mouse development, as the standard knockout (KO) results in early embryonic death. However, the role of HIRA in hematopoiesis is poorly understood. We investigated the effect of Hira KO on hematopoiesis using Vav-Cre Loxp system. We show that Hira KO dramatically reduces bone marrow LSK cells, resulting in anemia, thrombopenia and severe, combined immunodeficiency. To investigate the molecular mechanisms, RNA-seq and ATAC-Seq were performed using LSK cells isolated from WT and Hira conditional KO mice.

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Genome wide enrichment of H3.3 in WT and Hira-null embryonic stem cells and day 15 differentiated cardiac progenitor

Project description:HIRA is a histone chaperone that modulates gene expression through the deposition of H3.3. Conditional knockout of Hira in embryonic mouse hearts leads to cardiac septal defects. However, the effects of HIRA on the gene expression profile at earlier stages of cardiogenic mesoderm differentiation has not yet been studied. Differentiation of mouse embryonic stem cells (mESCs) towards cardiomyocytes mimics some of these events and is an accepted model of these early stages. We performed RNA-Seq and H3.3-HA ChIP-seq on both WT and Hira-null mESCs and early cardiomyocyte progenitors of both genotypes. Analysis of our RNA-seq data showed differential down regulation of cardiovascular development-related genes in Hira-null cardiomyocytes compared to WT cardiomyocytes. Correlating these data with H3.3 enrichment showed that HIRA is required for the expression of the transcription factors (TFs) Gata6, Meis1 and Tbx2. These TFs displayed diminished HIRA-dependent H3.3 enrichment in their gene bodies or at their transcription start site in the absence of HIRA. Our results reveal new transcription factors through which HIRA influences cardiogenesis in vitro and potentially in vivo.

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Project description:Sequencing of RNA isolated from the tibialis anterior muscles of 6 month old C57BL/6J mice that had been injected and electroporated with either a control non-targeting siRNA (NT) or two different UBR4 targeting siRNA sequences (UBR4 siRNA5 and siRNA7) to deplete UBR4. Muscles were harvested 7 days after electroporation and showed significant loss of UBR4 coincident with hypertrophy of type 2A and 2X myofibers.

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Genome-wide chromatin state in myoblasts lacking Hira [ChIP-seq]

Project description:The epigenetic mechanisms coordinating the maintenance of adult cellular lineages and the inhibition of alternative cell fates are poorly understood. Here we show that targeted ablation of the histone chaperone HIRA in myogenic cells leads to extensive transcriptional modifications consistent with a major role in maintaining skeletal muscle cellular identity. Conditional ablation of HIRA in muscle stem cells of adult mice compromised their capacity to regenerate and self-renew, leading to tissue repair failure. Epigenetic analysis of Hira-deficient cells showed a drastic reduction of histone variant H3.3 deposition and H3K27ac modification at regulatory regions of muscle genes. By contrast, genes from alternative lineages were ectopically expressed in Hira-mutant cells via MLL1/MLL2-mediated increase of H3K4me3 mark at silent promoter regions. Therefore, HIRA sustains the epigenetic landscape governing muscle cell lineage identity via incorporation of H3.3 at muscle gene regulatory regions, while preventing the expression of alternative lineage genes.

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