Mitofusin-2 is required for mouse oocyte meiotic maturation.

Jing-Hua Zhang,Xiu-Yan Yang,Fang-Fang Mo,Tian An,Guang-Jian Jiang,Na Yu Na Yu,Yu-Feng Li,Ke Wang,Teng Zhang,Si-Hua Gao,Ji-Wei Hu

doi:10.1038/srep30970

Abstract

Mitofusin-2 (Mfn2) is essential for embryonic development, anti-apoptotic events, protection against free radical-induced lesions, and mitochondrial fusion in many cells. However, little is known about its mechanism and function during oocyte maturation. In this study, we found that Mfn2 was expressed in the cytoplasm during different stages of mouse oocyte maturation. Mfn2 was mainly associated with α-tubulin during oocyte maturation. Knockdown of Mfn2 by specific siRNA injection into oocytes caused the mitochondrial morphology and quantity to change, resulting in severely defective spindles and misaligned chromosomes. This led to metaphase I arrest and the failure of first polar body extrusion. Furthermore, Mfn2 depletion from GV stage oocytes caused the redistribution of p38 MAPK in oocyte cytoplasm. These findings provide insights into potential mechanisms of Mfn2-mediated cellular alterations, which may have significant implications for oocyte maturation.

Highlights

Mitofusin-2 (Mfn2) is essential for embryonic development, anti-apoptotic events, protection against free radical-induced lesions, and mitochondrial fusion in many cells
Functional analysis of p38 mitogen-activated protein kinase (MAPK) in mouse oocytes suggests that this kinase regulates spindle assembly and accurate chromosome segregation through phosphorylation of MAPK-activated protein kinase[13,14]
Expression of Mfn[2] in germinal vesicle (GV) and ovulated MII oocytes was detected by the quantitative real-time polymerase chain reaction

Summary

Introduction

Mitofusin-2 (Mfn2) is essential for embryonic development, anti-apoptotic events, protection against free radical-induced lesions, and mitochondrial fusion in many cells. Knockdown of Mfn[2] by specific siRNA injection into oocytes caused the mitochondrial morphology and quantity to change, resulting in severely defective spindles and misaligned chromosomes. This led to metaphase I arrest and the failure of first polar body extrusion. Mfn[2] depletion from GV stage oocytes caused the redistribution of p38 MAPK in oocyte cytoplasm These findings provide insights into potential mechanisms of Mfn2-mediated cellular alterations, which may have significant implications for oocyte maturation. The first indication for this process is the disappearance of the GV as observed under the light microscope This change is called germinal vesicle breakdown (GVBD). The interactions remain unclear between Mfn[2] and p38 MAPK during oocyte maturation

Methods

Results

Conclusion