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Expression data from Lbx1-EGFP+ flow sorted cells from Pitx2 WT, HT, Null forelimb tissue

ABSTRACT: Determing the gene network regulated by Pitx2 in during forelimb muscle development of mouse embryos at E12.5. Lbx1 is coexpressed in Pitx2+ cells during forelimb development, thus Pitx2-LacZ and Lbx1-EGFP+ mice were cross bred to allow us to purify Lbx1-EGFP+|Pitx2 -wild type, het, or null cells by flow sorting We used microarray analysis to determine the genes misregulated in Pitx2 null mice compared to Pitx2 wild type and heterozygotes. Lbx1-EGFP+|Pitx2(+/+, LacZ/+, or LacZ/LacZ) cells were flow sorted, RNA extracted, labelled cDNA was hybridized to Affymetrix mouse genome 430 2.0 arrays

ORGANISM(S): Mus musculus

SUBMITTER: Adam Campbell

PROVIDER: E-GEOD-31945 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Prediction of gene network models in limb muscle precursors.

Campbell Adam L AL Eng Diana D Gross Michael K MK Kioussi Chrissa C

Gene 20120820 1

The ventrolateral dermomyotome gives rise to all muscles of the limbs through the delamination and migration of cells into the limb buds. These cells proliferate and form myoblasts, withdraw from the cell cycle and become terminally differentiated. The myogenic lineage colonizes pre-patterned regions to form muscle anlagen as muscle fibers are assembled. The regulatory mechanisms that control the later steps of this myogenic program are not well understood. The homeodomain transcription factor P ...[more]

PMID: 22917675

Similar Datasets

Expression data from Lbx1-EGFP+ flow sorted cells from Pitx2 WT, HT, Null forelimb tissue

Project description:Determing the gene network regulated by Pitx2 in during forelimb muscle development of mouse embryos at E12.5. Lbx1 is coexpressed in Pitx2+ cells during forelimb development, thus Pitx2-LacZ and Lbx1-EGFP+ mice were cross bred to allow us to purify Lbx1-EGFP+|Pitx2 -wildtype, het, or null cells by flow sorting We used microarray analysis to determine the genes misregulated in Pitx2 null mice compared to Pitx2 wildtype and heterozyogtes.

2013-06-11 | GSE31945 | GEO

Mus musculus

Project description:Expression data from Lbx1-EGFP+ flow sorted cells from Pitx2 WT, HT, Null forelimb tissue

| PRJNA145009 | ENA

Mapping the Chromatin State Dynamics in Myoblasts

Project description:The chromatin state in developing body parts provides a zip code to cellular populations that direct their cell fates. We used antibodies for H3K4me3, H3K27me3 and Pol2, to identify the chromatin state signature of the Pitx2-null mouse forelimb during mid-gestation, at embryonic day 12. The families of genes marked included those related to transcription, transcriptional regulation, and embryonic organ development. Transcription factors specific for muscle development were characterized by bivalent chromatin, as E12 is a transition time point from embryonic to fetal myogenesis. The identified chromatin state of muscle specific genes was in strong correlation with their observed expression profile. Examination of the histone marks H3K4me3, H3k27me3, and Pol2 in whole E12.5 forelimb tissues from Pitx2 null mice using the Illumina HiSeq 2000

2016-07-17 | E-GEOD-71128 | biostudies-arrayexpress

Conserved GTPase LepA (Elongation Factor 4) functions in biogenesis of the 30S subunit of the 70S ribosome

Project description:The physiological role of LepA, a paralog of EF-G found in all bacteria, has been a mystery for decades. Here, we show that LepA functions in ribosome biogenesis. In cells lacking LepA, immature 30S particles accumulate. Four proteins are specifically underrepresented in these particles-S3, S10, S14, and S21-all of which bind late in the assembly process and contribute to the folding of the 3' domain of 16S rRNA. Processing of 16S rRNA is also delayed in the mutant strain, as indicated by increased levels of precursor 17S rRNA in assembly intermediates. Mutation ΔlepA confers a synthetic growth phenotype in absence of RsgA, another GTPase, well known to act in 30S subunit assembly. Analysis of the ΔrsgA strain reveals accumulation of intermediates that resemble those seen in the absence of LepA. These data suggest that RsgA and LepA play partially redundant roles to ensure efficient 30S assembly. This data is published in paper PMID: 28096346

2019-07-03 | PXD014436 | Pride

Digit patterning is controlled by a Bmp-Sox9-Wnt Turing network modulated by morphogen gradients

Project description:The goal of this microarray analysis was to see which genes are differentially expressed between Sox9-EGFP positive cells and Sox9-EGFP negative cells in E11.5 mouse limb bud autopods of the reporter Sox9-EGFP knock-in mouse(Nakamura et al 2011). This was done in order to gain insight of the genes that could contribute to the specification of the digits (Sox9 positive cells). Mesenchymal cells were extracted from the mouse (Sox9EGFP knock-in, Nakamura et al . 2011) embryo forelimb autopod at stage E11.5. Sox9EGFP-positive cells were FACS-sorted from Sox9EGFP-negative cells . Each FACS-sorted sample was made from several forelimb autopods (approximately n=10). Three replicates were used for each group of Sox9EGFP-positive cells and Sox9EGFP-negative cells. Extraction of total RNA, labeling and hybridization to the microarray were performed using attached protocols. We identified the genes that were differentially expressed between the two groups.

2014-06-15 | E-GEOD-58158 | biostudies-arrayexpress

MYBQKI overexpression in mouse NSC, and suppression of wild type Qk

Project description:Samples are mouse neural stem cells overexpressing eGFP, MYBtr, MYBQKI5, MYBQKI6 and MYBQKI6 with suppression of Qk (or LacZ)

2015-12-31 | GSE75796 | GEO

Gene expression data of postnatal Pitx2 deficient heart

Project description:Pitx2 is the homeobox gene located in proximity to the human 4q25 familial atrial fibrillation locus. Pitx2 haploinsufficient mice are prone to pacing induced atrial fibrillation indicating that reduced Pitx2 promotes an arrhythmogenic substrate within the atrium. Here, we inactivated Pitx2 in postnatal heart and discovered that unstressed adult Pitx2 mutant mice had sinus node dysfunction with impaired atrial conduction, an arrhythmia closely associated with atrial fibrillation. A genome-wide search for Pitx2 transcriptional targets using ChIP-sequencing and RNA expression profiling shows that Pitx2 represses target genes encoding cell junction proteins, ion channels, and critical transcriptional regulators many of which have been implicated in human atrial fibrillation by genome wide association studies. Pitx2 control and mutant hearts were collected from 3-, 6- and 12-week-old mice. At each time point, three cotrols and three mutants were collected as biological replicates. cDNA microarray analysis was performed using Affymetrix GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA).

2014-02-01 | E-GEOD-50399 | biostudies-arrayexpress

Patterns and mechanisms of ancestral histone protein inheritance in budding yeast

Project description:It is widely believed that chromatin, the nucleoprotein packaging state of eukaryotic genomes, can carry epigenetic information to propagate gene expression patterns in replicating cells. However, inheritance of genomic packaging status is subject to mechanistic challenges that do not confront the inheritance of genomic DNA sequence. Most notably, histone proteins must at least transiently dissociate from the maternal genome during replication, and it is unknown whether maternal proteins re-associate with daughter genomes near the sequence they originally occupied on the maternal genome. Here, we use a novel method for tracking old proteins to measure where histone proteins accumulate after 1, 3, or 6 generations of growth in yeast. To our surprise, ancestral histones accumulate near the 5M-bM-^@M-^Y end of long, relatively inactive genes. Using a mathematical model, we show that our results can be explained by the combined effects of histone replacement, histone movement along genes from 3M-bM-^@M-^Y to 5M-bM-^@M-^Y, and histone spreading during replication. Our results show that old histones do move, but stay relatively close (~400 bp) to their original location, which places important constraints on how chromatin could potentially carry epigenetic information. Our findings also suggest that accumulation of ancestral histones can influence histone modification patterns. Solexa/Illumina sequencing of H3-HA and H3-T7 MNase-ChIP. Samples of HA and T7 libraries were taken after the tag swap (a) before release from arrest (0 generations), (b) at 1, 3 and 6 cell divisions or (c) after 5 hours of G2/M arrest. Gene deletion mutants for (d) cac1 (e) top1 and (f) H4-tail deletion were taken after 3 cell divisions.

2011-10-06 | E-GEOD-28269 | biostudies-arrayexpress

Quaking is a global regulator of muscle-specific alternative splicing in vertebrates [siRNA data]

Project description:This work provides the first evidence that Qk is a global regulator of splicing in vertebrates, defines a new splicing regulatory network in muscle, and suggests that overlapping splicing networks contribute to the complexity of changes in alternative splicing during differentiation. Alternative splicing contributes to muscle development and differentiation, but the complete set of muscle splicing factors and their combinatorial interactions are not known. Previously work identifies ACUAA (STAR motif) as an enriched sequence near muscle-specific alternative exons such as Capzb exon 9. We did mass spectrometry of proteins selected by wild type and mutant Capzb intron 9 RNA affinity chromatography, and identified Quaking (Qk), a protein known to regulate mRNA function through ACUAA motifs in 3' UTRs. We show that in myoblasts, Qk promotes inclusion of Capzb exon 9 in opposition to repression by PTB. Qk knockdown in myoblasts has little effect on transcript levels, but alters inclusion of 824 cassette exons whose adjacent intron sequences are enriched in ACUAA motifs. During differentiation to myotubes, Qk levels increase 2-3 fold, suggesting a mechanism for Qk-responsive exon regulation. We captured the PTB splicing regulatory network and intersected it with the Qk network, identifying overlap between the functions of Qk and PTB. Approximately 60% of exons whose inclusion is altered during myogenesis appear to be under control of one or both of these splicing factors in myoblasts. This series is the C2C12 Qk and PTB siRNA data. It is 12 arrays: 3 PTB siRNA arrays , 3 Qk siRNA arrays, and 6 mock siRNA arrays.

2013-06-05 | E-GEOD-40961 | biostudies-arrayexpress

Mapping the Chromatin State Dynamics in Myoblasts

2016-07-17 | GSE71128 | GEO