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SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE114257 | GEO | 2021/07/29

REPOSITORIES: GEO

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SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ATAC-seq]

Project description:This study describes the functions of SMAD4 during early mouse limb bud development by identifying the direct transcriptional targets

2021-07-29 | GSE114255 | GEO

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ChIP-seq]

Project description:This study describes the functions of SMAD4 during early mouse limb bud development by identifying the direct transcriptional targets

2021-07-29 | GSE114253 | GEO

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [RNA-seq]

Project description:This study describes the functions of SMAD4 during early mouse limb bud development by identifying the direct transcriptional targets

2021-07-29 | GSE114252 | GEO

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds

Project description:SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds

| PRJNA470673 | ENA

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ChIP-seq]

Project description:SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ChIP-seq]

| PRJNA470681 | ENA

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ATAC-seq]

Project description:SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [ATAC-seq]

| PRJNA470678 | ENA

SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [RNA-seq]

Project description:SMAD4 Controls Morphogenetic SHH Signaling via Direct Transcriptional Regulation of Cholesterol Biosynthesis in Early Mouse Limb Buds [RNA-seq]

| PRJNA470680 | ENA

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

FGF-regulated Etv genes are essential for repressing Shh expression in mouse limb buds.

Project description:Anterior-posterior (A-P) patterning of the vertebrate limb is controlled by sonic hedgehog (SHH) signaling, and the precise restriction of Shh expression to the posterior limb bud is essential for its polarizing effect. Fibroblast growth factor (FGF) signaling, a key control of proximal-distal (P-D) limb outgrowth, is known to promote Shh expression in the posterior limb bud. Here, we show that conditional knockout of the FGF-activated transcription factor genes Etv4 and Etv5 in mouse led to ectopic Shh expression in the anterior limb bud and a preaxial polydactyly (PPD) skeletal phenotype. These unexpected results suggest that ETV4 and ETV5 act downstream of FGF signaling to inhibit Shh expression in the anterior limb bud. This finding elucidates a novel aspect of the mechanism coordinating limb development along the A-P and P-D axes.

| S-EPMC3541528 | biostudies-literature

Cholesterol modification restricts the spread of Shh gradient in the limb bud.

Project description:Sonic hedgehog (Shh) produced in the zone of polarizing activity is the major determinant of anteroposterior development of the amniote limb. The mature and active Shh protein is cholesterol-modified at its C terminus, and the hydrophobic nature of the modification requires the function of Dispatched (mDispA), a seven-pass transmembrane protein, for Shh release from its source. The current model suggests that the cholesterol moiety promotes the spread of Shh gradient in the limb bud. However, this model is inconsistent with findings in Drosophila and not in line with current thoughts on the role of the cholesterol moiety in Shh multimerization. Therefore, it remains unclear how the cholesterol moiety affects the postrelease extracellular behavior of Shh that relates to the shape of its activity gradient in responsive tissues. Here, we report functional analyses in mice showing that Shh lacking cholesterol modification (ShhN) has an increased propensity to spread long-distance, eliciting ectopic Shh pathway activation consistent with target gene expressions and modulating the level of Gli3 processing in the anterior limb mesoderm. These molecular alterations are reflected in the mispatterning of digits in ShhN mutants. Additionally, we provide direct evidence for the long-distance movement of ShhN across the anteroposterior axis of the limb bud. Our findings suggest that the cholesterol moiety regulates the range and shape of the Shh morphogen gradient by restricting rather than promoting the postrelease spread of Shh across the limb bud during early development.

| S-EPMC1458921 | biostudies-literature

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