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Expression data from E11.5 mouse embryonic forelimbs - various mutant conditions or dissected limb domains

ABSTRACT: Sonic hedgehog (Shh) signals via Gli transcription factors to direct digit number and identity in the vertebrate limb. We have characterized the Gli-dependent cis-regulatory network through a combination of whole genome ChIP-on-chip and transcriptional profiling of the developing mouse limb. In this dataset, we include the expression data obtained from dissected mouse forelimbs using a variety of gain- and loss-of-function hedgehog pathway mutants, as well as limbs dissected into responsive (posterior 2/3ds) and non-responsive (anterior 1/3d) Hh tissues. These data are used to obtain 753 genes that are differentially expressed in response to Shh signaling. Keywords: Comparison of genetic samples

ORGANISM(S): Mus musculus

PROVIDER: GSE11063 | GEO | 2008/09/15

SECONDARY ACCESSION(S): PRJNA108817

REPOSITORIES: GEO

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Expression data from E11.5 mouse embryonic forelimbs - various mutant conditions or dissected limb domains

Project description:Sonic hedgehog (Shh) signals via Gli transcription factors to direct digit number and identity in the vertebrate limb. We have characterized the Gli-dependent cis-regulatory network through a combination of whole genome ChIP-on-chip and transcriptional profiling of the developing mouse limb. In this dataset, we include the expression data obtained from dissected mouse forelimbs using a variety of gain- and loss-of-function hedgehog pathway mutants, as well as limbs dissected into responsive (posterior 2/3ds) and non-responsive (anterior 1/3d) Hh tissues. These data are used to obtain 753 genes that are differentially expressed in response to Shh signaling. Keywords: Comparison of genetic samples 28 Total samples were analyzed. We generated the following pairwise comparisons using PowerExpress: Shh<WT; SmoM2>WT; Gli3<WT; Gli3>WT; Ant<Post; Ant>Post. Genes with an FDRM-bM-^IM-$10% and a fold-change M-bM-^IM-%2 were selected. We did not generate pairwise comparisons for a certain combinations with SmoGli3 and Gli3 mutants because data from these arrays contained significant variability. To identify additional genes that were Shh-responsive, we performed the following multiple sample comparisons using an FDRM-bM-^IM-$10% and a posterior probability cutoff of M-bM-^IM-$25%: 1.) Ant<Post and Shh<WT<SmoM2, 2.) Ant<Post and Shh<WT<SmoM2 and Gli3>SmoGli3, 3.) Ant<Post and Shh<WT<SmoM2 and WT>SmoGli3

2008-09-14 | E-GEOD-11063 | biostudies-arrayexpress

Expression data from E12 mouse lumbar motor neuron subsets

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Expression data from adult male mouse hypothalamus

Project description:Laser captured regions surrounding the perifornical area (PeFA) in adult male mice that attacked pups; a control outside region (unk); a c-fos positive region (c-fos); an oxytocin positive region (oxt) In this dataset, we include the expression data obtained from dissected mouse forelimbs using a variety of gain- and loss-of-function hedgehog pathway mutants, as well as limbs dissected into responsive (posterior 2/3ds) and non-responsive (anterior 1/3d) Hh tissues. These data are used to obtain 753 genes that are differentially expressed in response to Shh signaling.

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Genome wide maps of chromatin modification in response to Hh signaling in mouse embryonic forelimb buds

Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers and the majority of Hh targets in the developing limb bud are regulated solely by the activity of GLI-repressor. Currently we do not have a comprehensive understanding of how GLI bound enhancers respond Hedgehog signaling. The goal of this study is to identify how GLI bound enhancers are regulated by Hedgehog signaling and specifically by GLI-repressor. Methods: Histone modification ChIP-sequencing was done in Embryonic day 10.5 limb buds from control and Shh null embryos to identify histone modifications that change in response to Hedgehog signaling. We also did a comparative analysis of histone modificaiton response to Hedgehog stimulation in NIH3T3 cells to assess tissue specificity of GLI bound enhancer response to Hedgehog signaling. Results: We found that Hedgehog signaling specifically regulates the acetylation status of Histone 3 lysine 27 at a subset of GLI binding regions. These regions correlate with both known Hedgehog target genes in the limb bud and with characterized enhancers in the limb. This set of Hedgehog responsive GLI bound enhancers demonstrate enhanced tissue specificity.

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RNA sequencing of cultured mouse wild-type E10.25 forelimbs in control or cyclopmaine containing media [SOLiD]

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RNA sequencing of cultured mouse wild-type E10.25 forelimbs in control or cyclopmaine containing media [SOLiD]

Project description:We wanted to identify differentially expressed genes in wild-type forelimbs and forelimbs briefly exposed to Shh signaling. E10.25 forelimbs were cultured in control media and media containing cyclopmaine (inhibits the Hedgehog pathway) Generated two wild-type (control) and two cyclopmaine biological replicates for RNA-seq UT-Genome and Analysis Facility

2015-07-01 | E-GEOD-58664 | biostudies-arrayexpress

Genome-wide maps of chromatin accessibility in response to Hh signaling in mouse embryonic forelimb buds

Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers and the majority of Hh targets in the developing limb bud are regulated solely by the activity of GLI-repressor. Currently, we do not have a comprehensive understanding of how GLI bound enhancers respond to Hedgehog signaling. The goal of this study is to identify how GLI bound enhancers are regulated by Hedgehog signaling and specifically by GLI-repressor. Methods: ATAC-seq was done in embryonic day 10.5 posterior limb buds from control and Shh-null embryos to identify GLI enhancers that change chromatin accessibility in response to Hedgehog signaling. Results: We found that Hedgehog signaling regulates the chromatin accessibility of a subset of GLI binding regions. This subset of GLI bound enhancers has reduced accessibility in the absence of Hedgehog signaling and largely overlaps with GLI enhancers that also have reduced H3K27ac in the absence of Hedgehog signaling.

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H3K27ac in WT and Shh-/-, and Shh-/-;Gli3-/- E10.5 limb buds

Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers. While most Hh targets in the developing limb bud appear to be regulated by the activity of GLI-repressor, the role of GLI activator in this regulation is unclear. Here we assess the roles of GLI activator and repressor in regulating H3K27ac to activate their enhancers. Methods: ChIP-seq was performed in Embryonic day 10.5 mouse limb buds from WT, Shh-/- and Shh-/-Gli3-/- embryos Results: We found that most GLI binding regions can be activated in the absence of both GLI activator and repressor, while a small subset require GLI activator for activity. These indicate that most GLI enhancers in the limb are regulated by GLI repression.

2020-01-21 | GSE133712 | GEO

ChIP-seq analysis of Gli1 and Sox2 input to neural progenitor program and integration with actve histone marks

Project description:In the vertebrate neural tube, regional Sonic hedgehog (Shh) signaling invokes a time- and concentration-dependent induction of six different cell populations mediated through Gli transcriptional regulators. Elsewhere in the embryo, Shh/Gli responses invoke different tissue appropriate regulatory programs. To elucidate Shh/Gli regulation of neural fate sepcification, we performed Gli1 ChIP-Seq analysis. We further analyzed two transcription factors whose motifs were enriched in Gli1 ChIP data (Sox2 and Foxa2). Two active histone marks (H3K4me2 and H3K27ac) were additionally analyzed to study activity status of Shh-responsive cis-elements.

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ChIP-seq analysis of Gli1 and Sox2 input to neural progenitor program and integration with actve histone marks

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