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Research Paper|Volume 11, Issue 12|pp 3919—3938

Mitofusin 2 plays a role in oocyte and follicle development, and is required to maintain ovarian follicular reserve during reproductive aging

Man Zhang1, Muhammed Burak Bener1, Zongliang Jiang1,3, Tianren Wang1,4, Ecem Esencan1, Richard Scott III1, Tamas Horvath1,2, Emre Seli1
  • 1Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06510, USA
  • 2Department of Comparative Medicine, Yale School of Medicine, New Haven, CT 06520, USA
  • 3Current address: AgCenter, School of Animal Sciences, Louisiana State University, Baton Rouge, LA 70803, USA
  • 4Current address: Foundation for Embryonic Competence, Basking Ridge, NJ 07920, USA
Received: April 18, 2019Accepted: June 8, 2019Published: June 16, 2019
https://doi.org/10.18632/aging.102024

Copyright: Zhang et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Mitochondria change their shape through fusion and fission in order to adapt to their metabolic milieu. Mitofusin-2 (MFN2) is a key regulatory protein in this process, mediating mitochondrial fusion and interaction with endoplasmic reticulum. Targeted deletion of Mfn2 in oocytes resulted in mitochondrial dysfunction and female subfertility associated with impaired oocyte maturation and follicle development. Oocytes lacking MFN2 showed shortened telomeres and increased apoptosis, resulting in compromised oocyte quality and accelerated follicular depletion, consistent with a reproductive aging phenotype.