Mitochondrial Calcium uniporters are essential for meiotic progression in mouse oocytes by controlling Ca2+ entry
文献类型： 外文期刊
作者： Lu Yao Zhang 1 ; Meng Lin 1 ; Zhuan Qingrui 2 ; Wang Zichuan 1 ; Li Junjin 1 ; Liu Kexiong 1 ; Fu Xiangwei 2 ; Hou Yunpen 1 ;
作者机构： 1.China Agr Univ, Coll Biol Sci, State Key Labs Agrobiotechnol, 2 Yuanmingyuan Xilu, Beijing 100193, Peoples R China
2.China Agr Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod, Beijing, Peoples R China
3.Xinjiang Acad Agr & Reclamat Sci, State Key Lab Sheep Genet Improvement & Hlth Bree, Shihezi, Peoples R China
关键词： AMPK; meiosis; mitochondrial Ca2+; mitochondrial function; oocytes
期刊名称：CELL PROLIFERATION （ 影响因子：6.831； 五年影响因子：6.154 ）
ISSN： 0960-7722
年卷期： 2021 年 54 卷 11 期
页码：
收录情况： SCI
摘要： Objectives The alteration of bioenergetics by oocytes in response to the demands of various biological processes plays a critical role in maintaining normal cellular physiology. However, little is known about the association between energy sensing and energy production with energy-dependent cellular processes like meiosis. Materials and methods We demonstrated that cell cycle-dependent mitochondrial Ca2+ connects energy sensing to mitochondrial activity in meiosis progression within mouse oocytes. Further, we established a model in mouse oocytes using siRNA knockdowns that target mitochondrial calcium uniporters (MCUs) in order to inhibit mitochondrial Ca2+ concentrations. Results Decreased numbers of oocytes successfully progressed to the germinal vesicle stage and extruded the first polar body during in vitro culture after inhibition, while spindle checkpoint-dependent meiosis was also delayed. Mitochondrial Ca2+ levels changed, and this was followed by altered mitochondrial masses and ATP levels within oocytes during the entirety of meiosis progression. Abnormal mitochondrial Ca2+ concentrations in oocytes then hindered meiotic progress and activated AMP-activated protein kinase (AMPK) signalling that is associated with gene expression. Conclusions These data provide new insight into the protective role that MCU-dependent mitochondrial Ca2+ signalling plays in meiotic progress, in addition to demonstrating a new mechanism of mitochondrial energy regulation by AMPK signalling that influences meiotic maturation.
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