MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells

Amir Bahat, Andres Goldman, Yehudit Zaltsman, Dilshad H. Khan, Coral Halperin, Emmanuel Amzallag, Vladislav Krupalnik, Michael Mullokandov, Alon Silberman, Ayelet Erez, Aaron D. Schimmer, Jacob H. Hanna and Atan Gross ()
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Amir Bahat: Weizmann Institute of Science
Andres Goldman: Weizmann Institute of Science
Yehudit Zaltsman: Weizmann Institute of Science
Dilshad H. Khan: University Health Network
Coral Halperin: Weizmann Institute of Science
Emmanuel Amzallag: Weizmann Institute of Science
Vladislav Krupalnik: Weizmann Institute of Science
Michael Mullokandov: Weizmann Institute of Science
Alon Silberman: Weizmann Institute of Science
Ayelet Erez: Weizmann Institute of Science
Aaron D. Schimmer: University Health Network
Jacob H. Hanna: Weizmann Institute of Science
Atan Gross: Weizmann Institute of Science

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract The role of mitochondria dynamics and its molecular regulators remains largely unknown during naïve-to-primed pluripotent cell interconversion. Here we report that mitochondrial MTCH2 is a regulator of mitochondrial fusion, essential for the naïve-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 naïve 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 naïve 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 naïve-to-primed pluripotency interconversion of murine ESCs.

Date: 2018
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DOI: 10.1038/s41467-018-07519-w

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