Genomics

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A Cdx4-Sall4 regulatory module controls the transition from mesoderm formation to embryonic hematopoiesis


ABSTRACT: 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.

ORGANISM(S): Danio rerio  

SUBMITTER: Shaun Mahony  David K Gifford   Alan J Davidson   Richard M White   Bilguujin Dorjsuren   Christian Mosimann   Anthony DiBiase   Elizabeth J Paik   Leonard I Zon   Emily N Price    

PROVIDER: E-GEOD-48254 | ArrayExpress | 2013-12-02

SECONDARY ACCESSION(S): GSE48254SRP026282PRJNA209381

REPOSITORIES: GEO, ArrayExpress, ENA

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A Cdx4-Sall4 regulatory module controls the transition from mesoderm formation to embryonic hematopoiesis.

Paik Elizabeth J EJ   Mahony Shaun S   White Richard M RM   Price Emily N EN   Dibiase Anthony A   Dorjsuren Bilguujin B   Mosimann Christian C   Davidson Alan J AJ   Gifford David D   Zon Leonard I LI  

Stem cell reports 20131107 5


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 chromatin immunoprecipitation sequencing (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 th  ...[more]

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