Abstract
BackgroundRex1/Zfp42 has been extensively used as a marker for the undifferentiated state of pluripotent stem cells. However, its function in pluripotent stem cells including embryonic stem (ES) cells remained unclear although its involvement in visceral endoderm differentiation in F9 embryonal carcinoma (EC) cells was reported.ResultsWe showed the function of Rex1 in mouse ES cells as well as in embryos using the conventional gene targeting strategy. Our results clearly indicated that Rex1 function is dispensable for both the maintenance of pluripotency in ES cells and the development of embryos. However, Rex1-/- ES cells showed the defect to induce a subset of the marker genes of visceral endoderm, when differentiated as embryoid body, as found in EC cells.ConclusionRex1 should be regarded just as a marker of pluripotency without functional significance like the activity of alkaline phosphatase.
Highlights
Rex1/Zfp42 has been extensively used as a marker for the undifferentiated state of pluripotent stem cells
Generation of gain- and loss-of-function mutant embryonic stem (ES) cell lines for Rex1 To analyze the precise function of Rex1 in the maintenance of pluripotency, we generated a series of genetically-engineered ES cell lines for its gain- and loss-of function analyses
Multiple Rex1-/- ES cell lines were established with extremely high efficiency (4 of 4 clones obtained after the selection were homozygous for Rex1 KO allele)
Summary
Rex1/Zfp has been extensively used as a marker for the undifferentiated state of pluripotent stem cells. Pluripotency is the differentiation ability of a cell to give rise all embryonic and adult cell types. Studies of embryonic stem (ES) cells have revealed molecular mechanisms that govern pluripotency involving in both genetic and epigenetic mechanisms [1,2]. Three transcription factors Oct3/4, Sox and Nanog are regarded as pivotal regulators because the loss-of-function experiments confirmed their essential functions for maintenance of pluripotency in ES cells as well as in peri-implantation development [3,4,5,6,7]. Nanog overexpression supports self-renewal of mouse ES cells in the absence of leukemia inhibitory factor (LIF) and promote imposition of pluripotency on somatic cells after cellfusion with ES cells [8,9], whereas ectopic expression of Oct3/4 and Sox with additional two transcription factors Klf and cMyc is sufficient to induce pluripotency in embryonic and adult fibroblast cells [10]. Oct3/4 co-operates with Sox to activate transcription of the target genes (page number not for citation purposes)
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