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Expression data from cochlea isolated from Meis2 mutant and wild-type mice at E15

ABSTRACT: The aim of this study consists in detecting genes regulated by Meis2 in the murine cochlea In this data set we present 256 genes differentially regulated by Meis2 in the murine cochlea. These data serve as a platform for verifying their differential regulation by Meis2 via RNA in situ hybridisation or qPCR

ORGANISM(S): Mus musculus

PROVIDER: GSE149916 | GEO | 2020/05/06

REPOSITORIES: GEO

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Expression data from cochlea isolated from N-myc mutant and wild-type mice at E15

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Expression data from cochlea isolated from N-myc mutant and wild-type mice at E15

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Expression data from cochlea isolated from Meis2 mutant and wild-type mice at E15

Project description:Expression data from cochlea isolated from Meis2 mutant and wild-type mice at E15

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq mouse]

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [Affymetrix]

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Identifcation of Meis2 target genes in the otic cell line VOT-E36 via ChIP analysis

Project description:Meis genes have been shown to control essential processes during development of the central and peripheral nervous system. Here we have defined the roles of the Meis2 gene during vertebrate inner ear induction and the formation of the cochlea. Meis2 is expressed in several tissues required for inner ear induction and in non-sensory tissue of the cochlear duct. Global inactivation of Meis2 in the mouse leads to a severely reduced size of the otic vesicle. Tissue-specific knock outs of Meis2 reveal that its expression in the hindbrain is essential for inner ear induction. Inactivation of Meis2 in the inner ear itself leads to an aberrant coiling of the cochlear duct. By analyzing transcriptomes obtained from Meis2 mutants and ChIPseq analysis of an otic cell line we define candidate target genes for Meis2 which may be directly or indirectly involved in cochlear morphogenesis. Taken together, these data show that Meis2 is essential for inner ear formation and provide an entry point to unveil the network underlying proper coiling of the cochlear duct.

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq human]

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Meis2 ChIP-seq in palate

Project description:ChIP-Sequencing on Meis2-HA in E12.5 palate, to identify Meis2 binding chromatin regions and target genes. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.

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Analysis of the gene expression within the cochlea of aging C57BL6j mice.

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