Obesity-induced oocyte mitochondrial defects are partially prevented and rescued by supplementation with co-enzyme Q10 in a mouse model

Boots, Christina E.; Boudoures, Anna L.; Zhang, W.; Drury, Andrea; Moley, Kelle H.

doi:10.1093/humrep/dew181

Cited by 79 publications

(69 citation statements)

References 27 publications

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“…The main effect of the OreR nuclear genome to disrupt oogenesis, but not larval development, is consistent with the known tissue-specific characteristics of other metabolic dysfunctions in development and disease, and the sensitivity of oogenesis to metabolic stress, including that caused by mitochondrial dysfunction (Benkhalifa et al, 2014;Bentov et al, 2011;Boots et al, 2016;Grindler and Moley, 2013;McCall, 2004;Morrison and Spradling, 2008;Sieber et al, 2016). Although our rescue experiments showed that the allelic incompatibility between the Aatm V allele and simw 501 mitochondria causes the maternal effect embryonic lethality, preliminary observations suggest that the ovarian failure phenotype is multigenic and not just determined by alleles of Aatm.…”

Section: Discussionsupporting

confidence: 77%

Incompatibility between mitochondrial and nuclear genomes during oogenesis results in ovarian failure and embryonic lethality

2017

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Mitochondrial dysfunction can cause female infertility. An important unresolved issue is the extent to which incompatibility between mitochondrial and nuclear genomes contributes to female infertility. It has previously been shown that a mitochondrial haplotype from D. simulans (simw 501) is incompatible with a nuclear genome from the D. melanogaster strain Oregon-R (OreR), resulting in impaired development, which was enhanced at higher temperature. This mitonuclear incompatibility is between alleles of the nuclear-encoded mitochondrial tyrosyl-tRNA synthetase (Aatm) and the mitochondrialencoded tyrosyl-tRNA that it aminoacylates. Here, we show that this mito-nuclear incompatibility causes a severe temperature-sensitive female infertility. The OreR nuclear genome contributed to death of ovarian germline stem cells and reduced egg production, which was further enhanced by the incompatibility with simw 501 mitochondria. Mito-nuclear incompatibility also resulted in aberrant egg morphology and a maternal-effect on embryonic chromosome segregation and survival, which was completely dependent on the temperature and mito-nuclear genotype of the mother. Our findings show that maternal mito-nuclear incompatibility during Drosophila oogenesis has severe consequences for egg production and embryonic survival, with important broader relevance to human female infertility and mitochondrial replacement therapy.

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Section: Discussionsupporting

confidence: 77%

Incompatibility between mitochondrial and nuclear genomes during oogenesis results in ovarian failure and embryonic lethality

2017

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“…In the reproductive system, ROS are mainly generated within the follicle and ovulation also produces ROS . Localization of mitochondria inside the oocyte is also associated with its developmental competence …”

Section: Introductionmentioning

confidence: 99%

Fenoxaprop‐ethyl affects mouse oocyte quality and the underlying mechanisms

Yang

Zhao

et al. 2018

Pest Management Science

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“…It is proved that microtubule defect can result in meiotic nondisjunction in oocytes. Several studies indicate that aberrant spindle assemble and chromosome misalignment participate in impairing the female reproduction ability in various species . Also, disrupted spindle assembly and misaligned chromosomes are supposed to be related to producing aneuploidy oocytes, which are important during infertility .…”

Section: Discussionmentioning

confidence: 99%

Tributyltin oxide exposure impairs mouse oocyte maturation and its possible mechanisms

Yang

Cui

et al. 2018

J of Cellular Biochemistry

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Tributyltin oxide (TBTO) has been widely used as marine antifouling composition, preservative, biocide, and a stabilizer in plastic industry. Previous studies have indicated that TBTO can cause immunotoxicity as an environmental pollutant. However, little is known about its reproductive toxicity, especially on female oocyte maturation and the underlying mechanisms. In this study, mouse oocytes were cultured with different concentrations of TBTO in vitro, and several crucial events during meiotic maturation were evaluated. We found that the first polar body extrusion rate was significantly reduced, which reflected the disruption of meiotic maturation. The rate of abnormal spindle organization increased significantly, accompanied with a higher rate of chromosome misalignment. In addition, TBTO treatment increased reactive oxygen species generation markedly, which also accelerated the early-stage apoptosis. Moreover, heterogeneous mitochondrial distribution, mitochondrial dysfunction, and higher rate of aneuploidy were detected, which consequently disrupted in vitro fertilization. In conclusion, our results indicated that TBTO exposure could impair mouse oocyte maturation by affecting spindle organization, chromosome alignment, mitochondria functions, oxidative stress, and apoptosis.

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Obesity-induced oocyte mitochondrial defects are partially prevented and rescued by supplementation with co-enzyme Q10 in a mouse model

Abstract: This study is not a clinical trial.

Cited by 79 publications

References 27 publications

Incompatibility between mitochondrial and nuclear genomes during oogenesis results in ovarian failure and embryonic lethality

Incompatibility between mitochondrial and nuclear genomes during oogenesis results in ovarian failure and embryonic lethality

Fenoxaprop‐ethyl affects mouse oocyte quality and the underlying mechanisms

Tributyltin oxide exposure impairs mouse oocyte maturation and its possible mechanisms

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