Oocyte ageing and its cellular basis

Eichenlaub-Ritter, Ursula

doi:10.1387/ijdb.120141ue

Cited by 103 publications

(65 citation statements)

References 95 publications

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“…The frequencies of large mitochondrial deletions (38) and the T414G mutation (39) were shown to increase in oocytes as a function of age-consistent with altered mitochondrial cytochemistry and a mutagenic environment with increased glycation and carbonyl stress in aging oocytes (40). However, the number of oocytes with defective mitochondria is significantly reduced during oogenesis (41).…”

Section: Estimating the Size Of The Germ-line Mtdna Bottleneck And Mumentioning

confidence: 94%

Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA

Rebolledo‐Jaramillo¹,

Su²,

Stoler³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

218

324

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The manifestation of mitochondrial DNA (mtDNA) diseases depends on the frequency of heteroplasmy (the presence of several alleles in an individual), yet its transmission across generations cannot be readily predicted owing to a lack of data on the size of the mtDNA bottleneck during oogenesis. For deleterious heteroplasmies, a severe bottleneck may abruptly transform a benign (low) frequency in a mother into a disease-causing (high) frequency in her child. Here we present a high-resolution study of heteroplasmy transmission conducted on blood and buccal mtDNA of 39 healthy mother-child pairs of European ancestry (a total of 156 samples, each sequenced at ∼20,000× per site). On average, each individual carried one heteroplasmy, and one in eight individuals carried a disease-associated heteroplasmy, with minor allele frequency ≥1%. We observed frequent drastic heteroplasmy frequency shifts between generations and estimated the effective size of the germline mtDNA bottleneck at only ∼30-35 (interquartile range from 9 to 141). Accounting for heteroplasmies, we estimated the mtDNA germ-line mutation rate at 1.3 × 10 −8 (interquartile range from 4.2 × 10 −9 to 4.1 × 10) mutations per site per year, an order of magnitude higher than for nuclear DNA. Notably, we found a positive association between the number of heteroplasmies in a child and maternal age at fertilization, likely attributable to oocyte aging. This study also took advantage of droplet digital PCR (ddPCR) to validate heteroplasmies and confirm a de novo mutation. Our results can be used to predict the transmission of disease-causing mtDNA variants and illuminate evolutionary dynamics of the mitochondrial genome. mitochondria | heteroplasmy

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Section: Estimating the Size Of The Germ-line Mtdna Bottleneck And Mumentioning

confidence: 94%

Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA

Rebolledo‐Jaramillo¹,

Su²,

Stoler³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

218

324

View full text Add to dashboard Cite

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“…Significantly, however, it has become apparent that the oocyte's SAC does not incorporate the same level of stringency in its ability to reliably monitor small numbers of misaligned chromosomes as is characteristic of mitosis (Nagaoka et al 2011, Gui & Homer 2012, Kolano et al 2012. For further details relating to SAC signal transduction in mammalian oocytes, the reader is referred to recent in-depth reviews (Homer 2011, Eichenlaub-Ritter 2012, Nagaoka et al 2012, Sun & Kim 2012.…”

Section: Apc/c-mediated Control Of M-phase Progressionmentioning

confidence: 99%

“…The intention here is to review current understanding of how the APC/C and its substrates take the mammalian oocyte through the gears of MI with a focus on recent developments, most of which relate to the Cdh1-activated species of APC/C (APC/C Cdh1 ) and its control of the G2-M transition and acentrosomal spindle assembly during prometaphase I. I also refer to the Cdc20-activated APC/C (APC/C Cdc20 ) but do not delve into great depth regarding its regulation by the spindle assembly checkpoint (SAC) as this has been the subject of recent excellent reviews (Homer 2011, Eichenlaub-Ritter 2012, Nagaoka et al 2012, Sun & Kim 2012.…”

Section: Introductionmentioning

confidence: 99%

The APC/C in female mammalian meiosis I

Homer¹

2013

Reproduction

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The anaphase-promoting complex or cyclosome (APC/C) orchestrates a meticulously controlled sequence of proteolytic events critical for proper cell cycle progression, the details of which have been most extensively elucidated during mitosis. It has become apparent, however, that the APC/C, particularly when acting in concert with its Cdh1 co-activator (APC/C Cdh1 ), executes a staggeringly diverse repertoire of functions that extend its remit well outside the bounds of mitosis. Findings over the past decade have not only earmarked mammalian oocyte maturation as one such case in point but have also begun to reveal a complex pattern of APC/C regulation that underpins many of the oocyte's unique developmental attributes. This review will encompass the latest findings pertinent to the APC/C, especially APC/C Cdh1 , in mammalian oocytes and how its activity and substrates shape the stop-start tempo of female mammalian first meiotic division and the challenging requirement for assembling spindles in the absence of centrosomes.Reproduction (2013) 146 R61-R71

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“…The overall high aneuploidy rates are increasing further with maternal age, at least in human and mouse oocytes [Eichenlaub-Ritter, 2012;Nagaoka et al, 2012;Jones and Lane, 2013;Herbert et al, 2015], although for example porcine oocytes do not show a similar age-related increase in aneuploidy [Hornak et al, 2011]. Despite the fact that we can explain the increase of aneuploidy coincidently with maternal age by deterioration of cohesion between sister chromatids [Chiang et al, 2010;Lister et al, 2010] due to the absence of turnover of the cohesin complex during a prolonged prophase arrest [Revenkova et al, 2010;Tachibana-Konwalski et al, 2010], we are still uncertain why the aneuploidy is so high even in oocytes from young individuals in comparison to meiosis in yeast and Drosophila [Hassold and Hunt, 2001].…”

mentioning

confidence: 99%

True Nondisjunction of Whole Bivalents in Oocytes with Attachment and Congression Defects

Šodek

Kovacovicova

Anger

2017

Cytogenet Genome Res

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Chromosome segregation in mammalian oocytes is prone to errors causing aneuploidy with consequences such as precocious termination of development or severe developmental disorders. Aneuploidy also represents a serious problem in procedures utilizing mammalian gametes and early embryos in vitro. In our study, we focused on congression defects during meiosis I and observed whole nondisjoined bivalents in meiosis II as a direct consequence, together with a substantially delayed first polar body extrusion. We also show that the congression defects are accompanied by less stable attachments of the kinetochores. Our results describe a process by which congression defects directly contribute to aneuploidy.

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Oocyte ageing and its cellular basis

Cited by 103 publications

References 95 publications

Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA

Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA

The APC/C in female mammalian meiosis I

True Nondisjunction of Whole Bivalents in Oocytes with Attachment and Congression Defects

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