{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang LY"],"funding":["The National Major Project for Production of Transgenic Breeding"],"pagination":["e13127"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8560604"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(11)"],"pubmed_abstract":["

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."],"journal":["Cell proliferation"],"pubmed_title":["Mitochondrial Calcium uniporters are essential for meiotic progression in mouse oocytes by controlling Ca2+ entry."],"pmcid":["PMC8560604"],"funding_grant_id":["2018ZX08007001"],"pubmed_authors":["Kexiong L","Zhang LY","Junjin L","Xiangwei F","Yunpeng H","Zichuan W","Lin M","Qingrui Z"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial Calcium uniporters are essential for meiotic progression in mouse oocytes by controlling Ca2+ entry.","description":"

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.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2024-11-05T22:36:11.405Z","creation":"2022-02-11T12:38:33.442Z"},"accession":"S-EPMC8560604","cross_references":{"pubmed":["34546582"],"doi":["10.1111/cpr.13127"]}}