西亚试剂：Aberrant silencing of imprinted genes on chromosome 12qF1 i

Aberrant silencing of imprinted genes on chromosome 12qF1 in mouse induced pluripotent stem cells
Matthias Stadtfeld1,2,3,7, Effie Apostolou1,2,3,7, Hidenori Akutsu4, Atsushi Fukuda5, Patricia Follett1, Sridaran Natesan6, Tomohiro Kono5, Toshi Shioda2 & Konrad Hochedlinger1,2,3

Howard Hughes Medical Institute at Massachusetts General Hospital, Center for Regenerative Medicine; Harvard Stem Cell Institute, 185 Cambridge Street, Boston, Massachusetts 02114, USA
Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
Department of Stem Cell and Regenerative Biology, Harvard University and Harvard Medical School, 42 Church Street, Cambridge, Massachusetts 02138, USA
Department of Reproductive Biology, National Institute for Child Health and Development, Tokyo 157-8535, Japan
Department of BioScience, Tokyo University of Agriculture, Tokyo 156-8502, Japan
Sanofi-Aventis, 270 Albany Street, Cambridge, Massachusetts 02139, USA
These authors contributed equally to this work.

Induced pluripotent stem cells (iPSCs) have been generated by enforced expression of defined sets of transcription factors in somatic cells. It remains controversial whether iPSCs are molecularly and functionally equivalent to blastocyst-derived embryonic stem (ES) cells. By comparing genetically identical mouse ES cells and iPSCs, we show here that their overall messenger RNA and microRNA expression patterns are indistinguishable with the exception of a few transcripts encoded within the imprinted Dlk1–Dio3 gene cluster on chromosome 12qF1, which were aberrantly silenced in most of the iPSC clones. Consistent with a developmental role of the Dlk1–Dio3 gene cluster, these iPSC clones contributed poorly to chimaeras and failed to support the development of entirely iPSC-derived animals (‘all-iPSC mice’). In contrast, iPSC clones with normal expression of the Dlk1–Dio3 cluster contributed to high-grade chimaeras and generated viable all-iPSC mice. Notably, treatment of an iPSC clone that had silenced Dlk1–Dio3 with a histone deacetylase inhibitor reactivated the locus and rescued its ability to support full-term development of all-iPSC mice. Thus, the expression state of a single imprinted gene cluster seems to distinguish most murine iPSCs from ES cells and allows for the prospective identification of iPSC clones that have the full development potential of ES cells.

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