Abstract
The principal factors that lead to proliferation and pluripotency in embryonic stem cells (ESCs) have been vigorously investigated. However, the global network of factors and their full signaling cascade is still unclear. In this study, we found that ECAT11 (L1td1) is one of the ESC-associated transcripts harboring a truncated fragment of ORF-1, a component of theL1 retrotransposable element. We generated an ECAT11 knock-in mouse by replacing its coding region with green fluorescent protein. In the early stage of development, the fluorescence was observed at the inner cell mass of blastocysts and epiblasts. Despite this specific expression, ECAT11-null mice grow normally and are fertile. In addition, ECAT11 was dispensable for both the proliferation and pluripotency of ESCs.We found rapid and robust activation of ECAT11 in fibroblasts after the forced expression of transcription factors that can give rise pluripotency in somatic cells.However, iPS cells could be established from ECAT11-null fibroblasts. Our data demonstrate thedispensability of ECAT11/L1td1 in pluripotency, despite its specific expression.
Highlights
Embryonic stem cells (ESCs) have been established from mammalian blastocysts [1],[2],[3]
We have shown that ECAT4 encodes the transcription factor Nanog, which plays critical roles in pluripotency [10], whereas ECAT5 encodes Eras, which promotes the proliferation of mouse ESCs [14]
We found that ECAT11 is rapidly activated by Oct3/4, Sox2 and Klf4 in fibroblasts, but is dispensable for the generation of induced pluripotent stem cells (iPSCs)
Summary
Embryonic stem cells (ESCs) have been established from mammalian blastocysts [1],[2],[3]. ESCs have the ability to proliferate vigorously and differentiate into various cell types. They are attractive sources for cell transplantation therapy and basic research. Induced pluripotent stem cells (iPSCs) were derived from mouse and human somatic cells that have similar differentiation potential to ESCs, and can overcome the ethical problems and immune rejection associated with ESCs [4],[5],[6]. In mouse ESCs, pluripotency can be maintained by leukemia inhibitory factor (LIF) and several transcription factors. Pluripotency is maintained by the regulatory networks of many transcription and other factors
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