Document Detail

Sall4 is essential for stabilization, but not for pluripotency, of embryonic stem cells by repressing aberrant trophectoderm gene expression.
MedLine Citation:
PMID:  19350679     Owner:  NLM     Status:  MEDLINE    
Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder Okihiro syndrome. We previously showed that the absence of Sall4 leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. Here, we report that, in the absence of feeder cells, Sall4-null ES cells express the trophectoderm marker Cdx2, but are maintained for a long period in an undifferentiated state with minimally affected Oct3/4 expression. Feeder-free Sall4-null ES cells contribute solely to the inner cell mass and epiblast in vivo, indicating that these cells still retain pluripotency and do not fully commit to the trophectoderm. These phenotypes could arise from derepression of the Cdx2 promoter, which is normally suppressed by Sall4 and the Mi2/NuRD HDAC complex. However, proliferation was impaired and G1 phase prolonged in the absence of Sall4, suggesting another role for Sall4 in cell cycle control. Although Sall1, also a Sall family gene, is known to genetically interact with Sall4 in vivo, Sall1-null ES cells have no apparent defects and no exacerbation is observed in ES cells lacking both Sall1 and Sall4, compared with Sall4-null cells. This suggests a unique role for Sall4 in ES cells. Thus, though Sall4 does not contribute to the central machinery of the pluripotency, it stabilizes ES cells by repressing aberrant trophectoderm gene expression.
Shunsuke Yuri; Sayoko Fujimura; Keisuke Nimura; Naoki Takeda; Yayoi Toyooka; Yu-Ichi Fujimura; Hiroyuki Aburatani; Kiyoe Ura; Haruhiko Koseki; Hitoshi Niwa; Ryuichi Nishinakamura
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Stem cells (Dayton, Ohio)     Volume:  27     ISSN:  1549-4918     ISO Abbreviation:  Stem Cells     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-23     Completed Date:  2009-06-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9304532     Medline TA:  Stem Cells     Country:  United States    
Other Details:
Languages:  eng     Pagination:  796-805     Citation Subset:  IM    
Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
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MeSH Terms
Cell Cycle / genetics
Cell Differentiation / physiology*
DNA-Binding Proteins / physiology*
Embryonic Development / genetics
Embryonic Stem Cells / physiology*
Gene Expression
Gene Expression Regulation, Developmental / physiology*
Homeodomain Proteins / genetics,  metabolism
Microscopy, Confocal
Oligonucleotide Array Sequence Analysis
Pluripotent Stem Cells / physiology*
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factors / physiology*
Reg. No./Substance:
0/CDX2 protein, human; 0/DNA-Binding Proteins; 0/Homeodomain Proteins; 0/Sall4 protein, mouse; 0/Transcription Factors

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