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Genome-wide transcription factor binding maps of glioma-associated oncogene family zinc finger 3 (Gli3) in Second Heart Field (SHF) cells disected from Mouse Embryos.

ABSTRACT: To investigate the heart development, the data were generated to examine the genome-wide Gli3 binding in SHF disected from Mouse Embryos.

ORGANISM(S): Mus musculus

PROVIDER: GSE44755 | GEO | 2013/03/01

SECONDARY ACCESSION(S): PRJNA191557

REPOSITORIES: GEO

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Genome-wide transcription factor binding maps of glioma-associated oncogene family zinc finger 3 (Gli3) in Second Heart Field (SHF) cells disected from Mouse Embryos.

Project description:To investigate the heart development, the data were generated to examine the genome-wide Gli3 binding in SHF disected from Mouse Embryos. Gli3 ChIP-Seq was compared to the input in SHF from mouse embryonic cells at E9.5.

2013-03-01 | E-GEOD-44755 | biostudies-arrayexpress

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Project description:Mutations in GLI3, which encodes a transcription factor of the Hedgehog signaling pathway, cause several developmental anomalies linked to inappropriate tissue patterning. Here, we report a novel missense variant in the fifth zinc finger domain of GLI3 (c.1826G>A; p.(Cys609Tyr)) initially identified in a proband with preaxial polydactyly type IV, developmental delay, sensorineural hearing loss, skeletal, and genitourinary anomalies. Additional family members exhibited various digital anomalies such as preaxial polydactyly, syndactyly, and postaxial polydactyly either in isolation or combined. Functional studies of Cys609Tyr GLI3 in cultured cells showed abnormal GLI3 processing leading to decreased GLI3 repressor production, increased basal transcriptional activity, and submaximal GLI reporter activity with Hedgehog pathway activation, thus demonstrating an intriguing molecular mechanism for this GLI3-related phenotype. Given the complexity of GLI3 post-translational processing and opposing biological functions as a transcriptional activator and repressor, our findings highlight the importance of performing functional studies of presumed GLI3 variants. This family also demonstrates how GLI3 variants are variably expressed.

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HDAC1-mediated repression of the retinoic acid-responsive gene ripply3 promotes second heart field development

Project description:Coordinated transcriptional and epigenetic mechanisms that direct development of the later differentiating second heart field (SHF) progenitors remain largely unknown. Here, we show that a novel zebrafish histone deacetylase 1 (hdac1) mutant allele cardiac really gone (crg) has a deficit of ventricular CMs and smooth muscle within the outflow tract (OFT) due to both cell and non-cell autonomous loss in SHF progenitor proliferation. Cyp26-deficient embryos, which have increased retinoic acid (RA) levels, have similar defects in SHF-derived OFT development. We found that nkx2.5+ progenitors from hdac1 and cyp26-deficient embryos have ectopic expression of ripply3, a transcriptional co-repressor of T-box transcription factors that is normally restricted to the posterior pharyngeal endoderm. Furthermore, the ripply3 expression domain is expanded anteriorly into the posterior nkx2.5+ progenitor domain in crg mutants. Importantly, excess ripply3 is sufficient to repress VC development, while genetic depletion of Ripply3 and Tbx1 in crg mutants can partially restore VC number. We find that in crg mutants the epigenetic signature at RA response elements (RAREs) that can associate with Hdac1 and RA receptors (RARs) becomes indicative of transcriptional activation. Our study highlights that transcriptional repression via the epigenetic regulator Hdac1 facilitates OFT development through directly preventing expression of the RA-responsive gene ripply3 within SHF progenitors.

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A Second Heart Field-derived vasculogenic niche contributes to cardiac lymphatics

Project description:The mammalian heart contains multiple cell types that appear progressively during embryonic development. Advances in determining cardiac lineage diversification has often been limited by the unreliability of genetic tracers. Here we combine clonal analysis, genetic lineage tracing, tissue transplantation and mutant characterization to investigate the lineage relationships between epicardium, arterial mesothelial cells (AMCs) and the coronary vasculature. We report a contribution of the second heart field (SHF) to a vasculogenic niche composed of AMCs and sub-mesothelial cells at the base of the pulmonary artery. Sub-mesothelial cells from this niche differentiate into lymphatic endothelial cells and, in close association with AMC-derived cells, contribute to, and are essential for the development of ventral cardiac lymphatics. In addition, regionalized epicardial/mesothelial retinoic acid signaling regulates lymphangiogenesis, contributing to the niche properties. These results uncover a SHF vasculogenic contribution to coronary lymphatic development through a local niche at the base of the great arteries.

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Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

Project description:Development of the vertebrate heart requires the appropriate integration of temporally-distinct differentiating progenitor populations. While factors that promote accrual of later-differentiating second heart field (SHF)-derived cells to the outflow tract (OFT) have been intensively investigated, few signals are understood that specifically restrict the size of the vertebrate OFT. Here, we show that improper specification and proliferation of SHF progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts with a specific increase in ventricular cardiomyocytes and smooth muscle cells within the OFT. Specifically, optogenetic lineage-tracing demonstrates Pbx4 initially promotes the proper partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arch arteries. Subsequently, Pbx4 also limits the size of the SHF through repressing SHF progenitor proliferation. Single-cell RNA sequencing of nkx2.5+ cells revealed that the enlarged SHF progenitor population within Pbx4-deficient embryos assimilates characteristics of normally distinct proliferative and more anterior, differentiated cardiomyocyte populations. Therefore, the generation of proper OFT size and great arteries in vertebrates requires Pbx-dependent stratification of unique progenitor differentiation states to facilitate homeotic-like transformations and limit progenitor production within the SHF.

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The BAF complex does not mediate GLI repression (Gli3 null Cut&RUN)

Project description:Purpose: This study seeks to determine whether GLI3 is required to recruit the SMARCC1 complex to GLI enhancers in the limb. Methods: To determine if Gli3 is required to recruit SMARCC1 to its anhancers, we performed differential chromatin binding to compare SMARCC1 binding in control and Gli3 mutants. We performed Cut&Run for SMARCC1 binding on individually genotyped E11.5 (40-43s) anterior forelimb pairs from control (Gli3+/+; 3 replicates) and Gli3 mutant (Gli3-/-; 4 replicates) embryos. Results: We found that there is no major difference in SMARCC1 binding in Gli3-mutants compared to controls.

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Project description:To study the effect of GLI3 knockout on early brain organoid development, we collected single-cell multiome data from 18 day old brain organoids

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