Identifcation of Meis2 target genes in the otic cell line VOT-E36 via ChIP analysis
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ABSTRACT:
PROVIDER: PRJNA699183 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13618913.fastq.gz | Fastqsanger.gz | |||
| SRR13618914.fastq.gz | Fastqsanger.gz |
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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.
2021-03-12 | GSE166072 | GEO
Project description:We report the RNAseq analysis of otic vesicles isolated from mouse wild-type and Meis2 mutant embryos at embryonic day 11.5 of development.
2020-07-21 | GSE154787 | GEO
Project description:The study of the gene expression during otic development is a source of important information for understanding the mechanism of inner ear development and subsequently create appropriate gene therapies both to prevent hearing loss and eventually to regenerate the damaged parts.This dataset contains data from temporal expression profiles in an epithelial cell line derived from the cochlear duct of a mouse inner ear at embryonic day E10.5. There are 6 time points across 14 days of in vitro differentiation in serum-free media. We used microarrays to define patterns of expression in a differentiating otic cell line. Experiment Overall Design: The model is based on the conditionally immortal cell line University of Sheffield/ventral otocyst-epithelial cell line clone 36 (US/VOT-E36), derived from ventral otic epithelial cells of the mouse at embryonic day 10.5. This cell ilines is recapitulates a coherent pattern of cell differentiation compared with in vivo cells and provide a convenient model for screening the effects of other extrinsic factors on the differentiation of cochlear epithelial cell types in vitro. The cell line VOT-E36 was weaned from the fetal calf serum (FCS), which was used to culture the parental cell line, by progressive serum dilution. The cell line was conditionally immortalized by a temperaturesensitive variant of the T antigen (tsA58), controlled by a c-interferoninducible promoter. Cell growth could then be arrested and the cells allowed to differentiate by culturing them at 39 C without c-interferon. Cultures were customarily set up under proliferative conditions (33 C, c-interferon) and allowed to grow for 2–3 days. To induce differentiation, the dishes were rinsed twice with Ultraculture and the medium was replaced without c-interferon and then transferred to 39 C. Medium was renewed every 4 days.
2009-04-17 | E-GEOD-15585 | biostudies-arrayexpress
Project description:Next generation sequencing of wild-type and Meis2 otic vesicle transcriptomes
| PRJNA647437 | ENA
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.
2020-03-23 | GSE143911 | GEO
Project description:Previously FGF signalling has been shown to specify otic fate from multipotent pre-placodal ectoderm. Though many FGF target genes have been identified in subsequent studies, none of them is sufficient to induce otic lineage. Profiling and analysing the transcriptome and epigenomical signature during otic specification, we predicted and confirmed Sox8 as an otic master regulator, able to specify otic fate in the pre-placodal ectoderm. This is achieved by activating the expression of otic identity markers and compromising the fate towards lens and trigeminal ganglion. In the combat to differentiate ESCs/iPSCs or convert other cell lineage into otic lineage, our discovery may add another weaponry to tame these cells towards otic cells.
2022-08-01 | GSE102825 | GEO
Project description:Calpains are non-lysosomal, Ca2+-dependent cysteine proteases, which are associated with various cellular functions but have so far been mainly studied in the context of disease. Their contribution to homeostasis in the healthy organism is still not well understood and their substrates have remained enigmatic in most cases. In the present study, we describe a previously unrecognized role for the calpain protease calpain2 in the regulation of neuronal differentiation of adult neural stem- and progenitor cells through cleavage and elimintation of the neuronal fate determinant MEIS2. Mass spectrometry analysis was performed on immunoprecipitated MEIS2 protein to identify phosphory¬lated residues in MEIS2 and on immunoprecipitated MEIS2 incubated with native porcine calpain2 to map calpain2-induced cleavage sites in the protein.
2024-02-08 | PXD036442 | Pride
Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program.
2012-12-12 | GSE42845 | GEO
Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program. 8 samples were analyzed. These contain two replicates of each of the following four catergories: Otic ectoderm, Non-Otic (lateral) ectoderm, Trigeminal Ectoderm cultured - FGF, Trigeminal Ectoderm cultured + FGF
2012-12-12 | E-GEOD-42845 | biostudies-arrayexpress
Project description:The study of the gene expression during otic development is a source of important information for understanding the mechanism of inner ear development and subsequently create appropriate gene therapies both to prevent hearing loss and eventually to regenerate the damaged parts.This dataset contains data from temporal expression profiles in an epithelial cell line derived from the cochlear duct of a mouse inner ear at embryonic day E10.5. There are 6 time points across 14 days of in vitro differentiation in serum-free media. We used microarrays to define patterns of expression in a differentiating otic cell line. Keywords: Temporal gene expression of 14 days of differentiation in vitro.
2009-04-08 | GSE15585 | GEO