AI Article Synopsis
- Elf5 is a key transcription factor for proper trophoblast development in mice, as its knockdown leads to increased differentiation of stem cells without affecting proliferation or cell death.
- Following Elf5 knockdown, the stem cells quickly lose expression of critical pluripotency genes (Sox2 and Sox3) and temporarily express Hand1, a gene linked to giant cell differentiation.
- The study indicates that Elf5 acts as a regulatory gatekeeper, preventing premature differentiation of extraembryonic ectoderm into trophoblasts, highlighting its essential role in maintaining stem cell properties during early development.
Article Abstract
In mice the transcription factor Elf5 is necessary for correct trophoblast development. Upon knockdown of Elf5, TS cells display neither a decrease in proliferation nor an increase in cell death but rather an increased propensity to differentiate. Such cells rapidly lose Sox2 and 3 expression, while transiently upregulating the giant cell differentiation determinant gene Hand1. Other genes affected within 24h of Elf5 knock-down, many of which have not previously been implicated in trophoblast development, exhibited in vivo expression domains and in vitro expression responses consistent with Elf5 having a role in counteracting trophoblast differentiation. In an ES to TS differentiation assay using Cdx2 overexpression with Elf5 loss of function cell lines, it was shown that Elf5 is necessary to prevent terminal trophoblast differentiation. This data thus suggest that Elf5 is a gatekeeper for the TS to differentiated trophoblast transition thereby preventing the precocious differentiation of the undifferentiated extraembryonic ectoderm.
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| http://dx.doi.org/10.1016/j.ydbio.2014.05.012 | DOI Listing |
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