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Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [ATAC-seq]

ABSTRACT: Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [ATAC-seq]

PROVIDER: PRJNA633173 | ENA |

REPOSITORIES: ENA

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Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [RNA-seq]

Project description:Vertebrate Hox genes are key players in the establishment of structures during the development of the main body axis. Subsequently, they play important roles either in organizing secondary axial structures such as the appendages, or during homeostasis in postnatal stages and adulthood. Here we set up to analyze their elusive function in the ectodermal compartment, using the mouse limb bud as a model. We report that the HoxC gene cluster was globally co-opted to be transcribed in the distal limb ectoderm, where it is activated following the rule of temporal colinearity. These ectodermal cells subsequently produce various keratinized organs such as nails or claws. Accordingly, deletion of the HoxC cluster led to mice lacking nails (anonychia) and also hairs (alopecia), a condition stronger than the previously reported loss of function of Hoxc13, which is causative of the ectodermal dysplasia 9 (ECTD9) syndrome in human patients. We further identified, in mammals only, two ectodermal-specific enhancers located upstream the gene cluster, which act synergistically to regulate Hoxc genes in these ectodermal organs. Deletion of these enhancers alone or in combination revealed a strong quantitative component in the regulation of these genes in the ectoderm, suggesting that these two enhancers may have evolved along with mammals to provide the level of HOXC proteins necessary for the full development of hairs and nails.

2020-10-05 | GSE150701 | GEO

Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [ATAC-seq]

2020-10-05 | GSE150700 | GEO

Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments

Project description:Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments

| PRJNA633172 | ENA

Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [RNA-seq]

Project description:Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments [RNA-seq]

| PRJNA633175 | ENA

Mammalian-specific ectodermal enhancers control the expression of <i>Hoxc</i> genes in developing nails and hair follicles.

Project description: Not available

| S-EPMC7720164 | biostudies-literature

Specific ectodermal enhancers control the expression of Hoxc genes in developing mammalian teguments

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-05 | GSE150702 | GEO

Extensive Functional Redundancy of Mammalian Enhancers

Project description:Extensive Functional Redundancy of Mammalian Enhancers

| PRJNA362215 | ENA

Identification of H3 Lysine 4 Monomethylation Associated Proteins at Mammalian Enhancers

Project description:Enhancers act to regulate cell type specific gene expression by facilitating the transcription of target genes. In mammalian cells active or primed enhancers are commonly marked by monomethylation of Histone H3 at lysine 4 (H3K4me1) in a cell-type specific manner. Whether and how this histone modification regulates enhancer-dependent transcription programs in mammals has been unclear. In the present study, we conducted SILAC Mass-spec experiments with mono-nucleosomes and identified multiple H3K4me1 associated proteins, including proteins involved in chromatin remodeling. We demonstrate that H3K4me1 augments the association of the chromatin remodeling complex BAF to enhancers in vivo. Furthermore we show that in vitro, H3K4me1 nucleosomes are more efficiently remodeled by the BAF complex. Crystal structures of a BAF component BAF45c further reveal that monomethylation, but not trimethylation, is accommodated in this protein’s H3K4 binding site. Our results suggest that H3K4me1 plays an active role at enhancers by facilitating the binding of the BAF complex and possibly other chromatin regulators.

2018-10-23 | PXD007942 | Pride

Self-organizing human neuruloids allow disease modeling in the developing ectodermal compartment

Project description:Self-organizing human neuruloids allow disease modeling in the developing ectodermal compartment

| PRJNA486449 | ENA

A novel long non-coding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1

Project description:Recently, increasing evidence shows that long noncoding RNAs (lncRNAs) play a significant role in human tumorigenesis. However, the function of lncRNAs in human gastric cancer remains largely unknown. By using publicly available expression profiling data from gastric cancer and integrating bioinformatics analyses, we screen and identify a novel lncRNA, HOXC-AS3. HOXC-AS3 is significantly increased in gastric cancer tissues and is correlated with clinical outcomes of gastric cancer. In addition, HOXC-AS3 regulates cell proliferation and migration both in vitro and in vivo. RNA-seq analysis reveals that HOXC-AS3 knockdown preferentially affects genes that are linked to proliferation and migration. Mechanistically, we find that HOXC-AS3 is obviously activated by gain of H3K4me3 and H3K27ac, both in cells and in tissues. RNA pull down-mass spectrometry analysis identifies that YBX1 interacts with HOXC-AS3, and RNA-seq analysis finds a marked overlap in genes differentially expressed after YBX1 knockdown and those transcriptionally regulated by HOXC-AS3, suggesting that YBX1 participates in HOXC-AS3-mediated gene transcriptional regulation in the tumorigenesis of gastric cancer.Together, our data demonstrate that abnormal histone modification-activated HOXC-AS3 may play important roles in gastric cancer oncogenesis and may serve as a target for gastric cancer diagnosis and therapy.

2018-08-26 | GSE119021 | GEO

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