A Cdx4-Sall4 regulatory module controls the transition from mesoderm formation to embryonic hematopoiesis
UID: 11068
- Description
- Description from Harvard Dataverse:
"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. (2013-11-19)"
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Access via GEO
Accession #: GSE48254Access via SRA
Accession #: SRP026282Access via BioProject
Accession #: PRJNA209381 - Access Restrictions
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Free to All
- Access Instructions
- Downloads available through Harvard Dataverse on a CC0 1.0 license, or through the NCBI Gene Expression Omnibus, BioProject, and SRA databases.
- DOI
- 10.7910/DVN/0XYJJW
- Associated Publications
- Equipment Used
- Software Used
- Dataset Format(s)
- TXT
- Dataset Size
- 12.4 KB
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