Zhongfu Ying

Abstract The mitochondrial unfolded protein response (UPRmt), a mitochondria-to-nucleus retrograde pathway that promotes the maintenance of mitochondrial function in response to stress, plays an important role in promoting lifespan extension in Caenorhabditis elegans1,2. However, its role in mammals, including its contributions to development or cell fate decisions, remains largely unexplored.

(Cell Metabolism 28, 935–945, e1–e5; December 4, 2018) In the originally published version of this article, in Figure 3A the H3K9me3 band was mistakenly reproduced as H3K27me1. The corrected version of Figure 3A is shown here. This mistake does not affect the conclusions of the paper. The error has now been corrected in the article online. The authors apologize for the error and any inconvenience that may have resulted.

Reprogramming of somatic cells to induced pluripotent stem cells reconfigures chromatin modifications. Whether and how this process is regulated by signals originating in the mitochondria remain unknown. Here we show that the mitochondrial permeability transition pore (mPTP), a key regulator of mitochondrial homeostasis, undergoes short-term opening during the early phase of reprogramming and that this transient activation enhances reprogramming.