Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209381 | ENA |
REPOSITORIES: ENA
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Project description:Deletion of caudal/cdx genes alters hox gene expression and causes defects in posterior tissues and hematopoiesis. Yet, the defects in hox gene expression only partially explain these phenotypes. To gain deeper insight into Cdx4 function, we performed ChIP-seq combined with gene expression profiling in zebrafish, and identified the transcription factor spalt-like 4 (sall4) as a Cdx4 target. ChIP-seq revealed that Sall4 bound to its own gene locus and the cdx4 locus. Expression profiling showed that Cdx4 and Sall4 co-regulate genes such as hox, scl, and lmo2 that initiate hematopoiesis. Combined cdx4/sall4 gene knock-down impairs erythropoiesis, and overexpression of the Cdx4 and Sall4 target genes scl and lmo2 together rescued the erythroid program. These findings suggest that auto- and cross- regulation of Cdx4 and Sall4 establish a stable molecular circuit in mesoderm that facilitates the activation of the blood-specific program as development proceeds. ChIP-seq was performed against Cdx4, Sall4, H3K27ac, and H3K4me3 in bud-stage zebrafish embryos. Input material was sequenced as controls.
2013-12-02 | E-GEOD-48254 | biostudies-arrayexpress
Project description:We performed differential DGE analysis on RNA-seq data to determine the genes misregulated in triple mutant embryos (3etv) for etv4, etv5a, and etv5b transcription factors. 3etv mutants had defects in posterior mesoderm formation, somitogenesis, and body axis straightening, as well as other Fgf related phenotypes.
2022-07-15 | GSE155013 | GEO
Project description:We performed differential DGE analysis on RNA-seq data to determine the genes misregulated in triple mutant embryos (3etv) for etv4, etv5a, and etv5b transcription factors. 3etv mutants had defects in posterior mesoderm formation, somitogenesis, and body axis straightening, as well as other Fgf related phenotypes.
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Project description:Deletion of caudal/cdx genes alters hox gene expression and causes defects in posterior tissues and hematopoiesis. Yet, the defects in hox gene expression only partially explain these phenotypes. To gain deeper insight into Cdx4 function, we performed ChIP-seq combined with gene expression profiling in zebrafish, and identified the transcription factor spalt-like 4 (sall4) as a Cdx4 target. ChIP-seq revealed that Sall4 bound to its own gene locus and the cdx4 locus. Expression profiling showed that Cdx4 and Sall4 co-regulate genes such as hox, scl, and lmo2 that initiate hematopoiesis. Combined cdx4/sall4 gene knock-down impairs erythropoiesis, and overexpression of the Cdx4 and Sall4 target genes scl and lmo2 together rescued the erythroid program. These findings suggest that auto- and cross- regulation of Cdx4 and Sall4 establish a stable molecular circuit in mesoderm that facilitates the activation of the blood-specific program as development proceeds.
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Project description:The trunk axial skeleton develops from paraxial mesoderm cells. Our recent study demonstrated that conditional knockout of the stem cell factor Sall4 in mice by TCre caused tail truncation and a disorganized axial skeleton posterior to the lumbar level. Based on this phenotype, we hypothesized that, in addition to the previously reported role of Sall4 in neuromesodermal progenitors, Sall4 is involved in the development of the paraxial mesoderm tissue. ATAC-seq in TCre; Sall4 mutant posterior trunk mesoderm shows that Sall4 knockout reduces chromatin accessibility. We found that Sall4- dependent open chromatin status drives activation and repression of WNT signaling activators and repressors, respectively, to promote WNT signaling. Moreover, footprinting analysis of ATAC-seq data suggests that Sall4-dependent chromatin accessibility facilitates CTCF binding, which contributes to the repression of neural genes within the mesoderm. This study unveils multiple mechanisms by which Sall4 regulates paraxial mesoderm development by directing activation of mesodermal genes and repression of neural genes.
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Project description:Spatiotemporal Analysis of Transcriptome in the paraxial mesoderm of zebrafish embryos
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