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Significance The development of iPSCs provides unprecedented opportunities for life sciences, drug discovery, and regenerative medicine. The efficiency of iPSC generation is quite low: typically less than 1% of human primary somatic cells that have received reprogramming factors turn into iPSCs. Previous studies revealed that cellular senescence was a major barrier to iPSC generation. In this study using human FOP mutant cells, we provide evidence that the BMP-SMAD-ID signaling suppressed p16/INK4A-mediated cellular senescence during the early phase in iPSC generation. These results are unexpected because BMP-SMAD signaling has negative effects on the self-renewal of human iPSCs. Here, we show that a human natural mutation increases the efficiency of iPSC generation.

BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence