| First Author | Bahat A | Year | 2018 |
| Journal | Nat Commun | Volume | 9 |
| Issue | 1 | Pages | 5132 |
| PubMed ID | 30510213 | Mgi Jnum | J:267823 |
| Mgi Id | MGI:6267820 | Doi | 10.1038/s41467-018-07519-w |
| Citation | Bahat A, et al. (2018) MTCH2-mediated mitochondrial fusion drives exit from naive pluripotency in embryonic stem cells. Nat Commun 9(1):5132 |
| abstractText | The role of mitochondria dynamics and its molecular regulators remains largely unknown during naive-to-primed pluripotent cell interconversion. Here we report that mitochondrial MTCH2 is a regulator of mitochondrial fusion, essential for the naive-to-primed interconversion of murine embryonic stem cells (ESCs). During this interconversion, wild-type ESCs elongate their mitochondria and slightly alter their glutamine utilization. In contrast, MTCH2(-/-) ESCs fail to elongate their mitochondria and to alter their metabolism, maintaining high levels of histone acetylation and expression of naive pluripotency markers. Importantly, enforced mitochondria elongation by the pro-fusion protein Mitofusin (MFN) 2 or by a dominant negative form of the pro-fission protein dynamin-related protein (DRP) 1 is sufficient to drive the exit from naive pluripotency of both MTCH2(-/-) and wild-type ESCs. Taken together, our data indicate that mitochondria elongation, governed by MTCH2, plays a critical role and constitutes an early driving force in the naive-to-primed pluripotency interconversion of murine ESCs. |
