HDAC1 binding regions in mouse embryonic limbs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA595550 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10690647.fastq.gz | Fastqsanger.gz | |||
| SRR10690648.fastq.gz | Fastqsanger.gz | |||
| SRR10690649.fastq.gz | Fastqsanger.gz | |||
| SRR10690650.fastq.gz | Fastqsanger.gz | |||
| SRR10690651.fastq.gz | Fastqsanger.gz |
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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: ChIP-seq was performed in Embryonic day 11.5 mouse forelimb and hidlimbs lfrom wildtype Swiss Webster mice. Results: We identified 15,347 HDAC1 binding sites in mouse E11.5 limb buds
2020-01-21 | GSE141998 | GEO
Project description:GLI3 binding regions in mouse embryonic forelimb buds
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Project description:Histone deacetylase 1 (HDAC1) is an enzyme that promotes deacetylation of acetylated lysine residues in histones and other proteins. Histone acetylation is often associated with gene activation and expression. Los of HDAC1 leads to severe problems in development and proliferation. Moreover, it seems to be the major histone deacetylase in mouse embryonic stem cells. We used microarrays to identify putative HDAC1 target genes. Experiment Overall Design: Wild type and HDAC1 mouse embryonic stem cell, originating from same litter, were used for RNA extraction and hybridization on Affymetrix microarrays.
2007-11-13 | E-GEOD-5583 | biostudies-arrayexpress
Project description:Histone deacetylase 1 and 2 (HDAC1/2) are the core catalytic components of co-repressor complexes which modulate gene expression. In most cell types, deletion of both Hdac1 and Hdac2 is required to generate a discernible phenotype, suggesting their activity is largely redundant. We have therefore generated an embryonic stem cell (ES) line in which Hdac1 and Hdac2 can be inactivated simultaneously using a Tamoxifen inducible CreER fusion. Loss of HDAC1/2 results in a 60% reduction in total HDAC activity and a loss of cell viability. Cell death is cell cycle dependent, since differentiated, non-proliferating cells, retain their viability. Furthermore, we observe increased mitotic defects, lagging chromosomes and micronuclei, suggesting HDAC1/2 maintain chromosomal stability. Consistent with a critical role in the regulation of gene expression, microarray analysis of Hdac1/2 deleted cells reveals 1,708 differentially expressed genes. Significantly for the maintenance of stem cell self-renewal, we detected a reduction in the expression of the pluripotent transcription factors, Oct4, Nanog and Rex1. HDAC1/2 activity is regulated through binding of inositol tetraphosphate molecule [Ins(1,4,5,6)P4] (IP4) sandwiched between the HDAC and its cognate co-repressor. This raises the important question of whether the IP4 actually regulates the activity of the complex in cells. By rescuing the viability of DKO cells, we demonstrate for the first time that mutations which abolish IP4 binding reduce the activity of HDAC1/2 in vivo. Our data indicate that HDAC1/2 have a generic, but essential role in cellular proliferation and regulate stem cell self-renewal by maintaining expression of key pluripotent transcription factors. Comparative gene expression profiles of wild type (Day 0) were compared to Hdac1lox/lox, Hdac2lox/lox; CreER ES cells on days 1, 2 and 3 following for OHT treatment using the Illumina mouseWG-6 v2 expression BeadChip platform. wild type (Day 0) were compared to Hdac1lox/lox, Hdac2lox/lox; CreER ES cells on days 1, 2 and 3 following for OHT treatment. Four time points were analyzed in triplicate.
2014-05-01 | E-GEOD-52134 | biostudies-arrayexpress
Project description:We analysed the composition of histone acetylase 1 (HDAC1)-associated proteins in different cellular backgrounds using quantitative mass spectrometry (MS). First, we affinity purified (AP) C-terminally FLAG-tagged HDAC1 from the nearly haploid human cell line HAP1 (Andersson et al, 1987). To examine cross-species conservation in the composition of HDAC1 complexes we additionally analysed HDAC1-FLAG purifications from mouse embryonic fibroblasts (MEFs). Genetic suppressor element 1 (GSE1) was identified as a prominent interaction partner of HDAC1. Hence, we purified V5-tagged GSE1 from HAP1 cells and analysed co-precipitated proteins.
2023-10-23 | PXD040307 | Pride
Project description:Histone deacetylase 1 and 2 (HDAC1/2) are the core catalytic components of co-repressor complexes which modulate gene expression. In most cell types, deletion of both Hdac1 and Hdac2 is required to generate a discernible phenotype, suggesting their activity is largely redundant. We have therefore generated an embryonic stem cell (ES) line in which Hdac1 and Hdac2 can be inactivated simultaneously using a Tamoxifen inducible CreER fusion. Loss of HDAC1/2 results in a 60% reduction in total HDAC activity and a loss of cell viability. Cell death is cell cycle dependent, since differentiated, non-proliferating cells, retain their viability. Furthermore, we observe increased mitotic defects, lagging chromosomes and micronuclei, suggesting HDAC1/2 maintain chromosomal stability. Consistent with a critical role in the regulation of gene expression, microarray analysis of Hdac1/2 deleted cells reveals 1,708 differentially expressed genes. Significantly for the maintenance of stem cell self-renewal, we detected a reduction in the expression of the pluripotent transcription factors, Oct4, Nanog and Rex1. HDAC1/2 activity is regulated through binding of inositol tetraphosphate molecule [Ins(1,4,5,6)P4] (IP4) sandwiched between the HDAC and its cognate co-repressor. This raises the important question of whether the IP4 actually regulates the activity of the complex in cells. By rescuing the viability of DKO cells, we demonstrate for the first time that mutations which abolish IP4 binding reduce the activity of HDAC1/2 in vivo. Our data indicate that HDAC1/2 have a generic, but essential role in cellular proliferation and regulate stem cell self-renewal by maintaining expression of key pluripotent transcription factors. Comparative gene expression profiles of wild type (Day 0) were compared to Hdac1lox/lox, Hdac2lox/lox; CreER ES cells on days 1, 2 and 3 following for OHT treatment using the Illumina mouseWG-6 v2 expression BeadChip platform.
2014-05-01 | GSE52134 | GEO
Project description:The development of vertebrate extremities is a complex process which requires a highly coordinated network of different transcriptional activities. The homeodomain transcription factor Shox2 is a key player in limb formation controlling neural, muscular and skeletal development. Here, we compared gene expression profiles of wildtype and Shox2 knockout limbs using microarray experiments to identify Shox2 target genes. Limbs of E12.5 mouse embryos were dissected, fore- and hindlimbs were pooled and genotyped for RNA extraction. RNA from 3 embryos of 2 different pregnancies (in total 6 embryos) was pooled per genotype (Wildtype and Shox2 Knockout) and compared.
2013-02-15 | E-GEOD-41945 | biostudies-arrayexpress
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: ChIP-seq was performed in Embryonic day 10.5 mouse limb buds from mice with endogenously FLAG tagged Gli3. Results: We identified 7282 GLI3 binding regions in the E10.5 limb bud.
2020-01-21 | GSE133710 | GEO
Project description:The morphologies of the amniote phallus and limbs differ dramatically, but these structures share signaling pathways and patterns of gene expression in early development. Thus far, the extent to which genital and limb transcriptional networks share cis-regulatory elements has remained unexplored. Using chromatin immunoprecipitation with an antibody against the histone modification mark H3K27ac followed by Illumina high-throughput sequencing, we identify thousands of active enhancers in developing limbs, genital tubercle, and additional embryonic tissues of the mouse and green anole lizard (Anolis carolinensis). We show in global analyses of cis-regulatory activity that embryonic limbs and genitalia display overlapping patterns of enhancer activity, and that many H3K27ac-marked regions are shared between mouse and green anole. Our findings support the hypothesis that the amniote phallus evolved through co-option of a preexisting appendage developmental program.
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