Promotion of direct reprogramming by transformation-deficient Myc

Masato Nakagawa, Nanako Takizawa, Megumi Narita, Tomoko Ichisaka, Shinya Yamanaka

Proceedings of the National Academy of Sciences · 2010 · 400 citations · 44 references

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TL;DR

Induced pluripotent stem cells are produced from fibroblasts by Oct3/4, Sox2, and Klf4, and while c‑Myc enhances reprogramming, it also raises tumor risk. The study shows that c‑Myc’s ability to promote iPSC generation is independent of its oncogenic transformation activity. Low‑transforming L‑Myc and c‑Myc mutants (W136E, dN2) reprogram human fibroblasts more efficiently than wild‑type c‑Myc, and in mice L‑Myc supports germline transmission without tumor formation, indicating distinct Myc domains mediate reprogramming versus transformation.

Abstract

Induced pluripotent stem cells (iPSCs) are generated from mouse and human fibroblasts by the introduction of three transcription factors: Oct3/4, Sox2, and Klf4. The proto-oncogene product c-Myc markedly promotes iPSC generation, but also increases tumor formation in iPSC-derived chimeric mice. We report that the promotion of iPSC generation by Myc is independent of its transformation property. We found that another Myc family member, L-Myc, as well as c-Myc mutants (W136E and dN2), all of which have little transformation activity, promoted human iPSC generation more efficiently and specifically compared with WT c-Myc. In mice, L-Myc promoted germline transmission, but not tumor formation, in the iPSC-derived chimeric mice. These data demonstrate that different functional moieties of the Myc proto-oncogene products are involved in the transformation and promotion of directed reprogramming.

References

44