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

Šodek, Martin; Kovacovicova, Kristina; Anger, Martin

doi:10.1159/000458513

Cited by 5 publications

(3 citation statements)

References 29 publications

(46 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also observed true non-disjunction (Fig. S2e) when severely misaligned bivalent segregated intact towards the nearest spindle pole (Sodek et al, 2017). Our data thus confirm previous reports that cohesion loss predisposes chromosomes to missegregation in aged oocytes and formally add the lagging chromosome (specifically Class-I) as a previously undefined route to aneuploidy.…”

Section: Discussionsupporting

confidence: 90%

Distinct classes of lagging chromosome underpin age-related oocyte aneuploidy in mouse

Mihajlović

Haverfield

FitzHarris

2021

Preprint

View full text Add to dashboard Cite

SUMMARYChromosome segregation errors that cause oocyte aneuploidy increase in frequency with maternal age and are considered a major contributing factor of age-related fertility decline in females. A common age-associated chromosome segregation phenomenon in oocytes is the lagging anaphase chromosome, but whether anaphase laggards actually missegregate and cause aneuploidy is unclear. Here we show unexpectedly that lagging chromosomes in mouse oocytes comprise two mechanistically distinct classes of motion that we refer to as ‘Class-I’ and ‘Class-II’. We use imaging approaches and mechanistic interventions to dissociate the two classes, and find that whereas Class-II laggards are benign, Class-I laggards can directly cause aneuploidy. Most notably, a controlled prolongation of meiosis-I specifically lessens Class-I lagging to prevent aneuploidy. Our data thus reveal lagging chromosomes to be a cause of age-related aneuploidy in mouse oocytes and suggest that manipulating the cell cycle could increase the yield of useful oocytes in some contexts.

show abstract

Section: Discussionsupporting

confidence: 90%

Distinct classes of lagging chromosome underpin age-related oocyte aneuploidy in mouse

Mihajlović

Haverfield

FitzHarris

2021

Preprint

View full text Add to dashboard Cite

show abstract

“…In contrast, MCAK showed significant asymmetry across the bivalents in the spretus hybrid, but not in control mus- culus oocytes (Figure 4B). The CPC localized all over the chromosomes in this hybrid without obvious enrichment on centromeres (Figure S4), probably due to higher levels of cohesin complex on chromosome arms (Sodek et al, 2017), which contributes to CPC recruitment through the Haspin kinase pathway (Goto et al, 2017). Therefore, we focused on MCAK as a MT-destabilizing factor in the spretus hybrid.…”

Section: Centromeres In An Interspecific Hybrid Exhibit Asymmetry In Destabilizers Governed By Condensinmentioning

confidence: 99%

Molecular Strategies of Meiotic Cheating by Selfish Centromeres

Akera

Trimm

Lampson

2019

Cell

101

119

View full text Add to dashboard Cite

show abstract

“…In contrast, MCAK showed significant asymmetry across the bivalents in the spretus hybrid, but not in control musculus oocytes ( Figure 4B). The CPC localized all over the chromosomes in this hybrid without obvious enrichment on centromeres ( Figure S4), probably due to higher levels of cohesin complex on chromosome arms (Sodek et al, 2017), which contributes to CPC recruitment through the Haspin kinase pathway (Goto et al, 2017). Therefore, we focused on MCAK as a MT-destabilizing factor in the spretus hybrid.…”

Section: Centromeres In An Interspecific Hybrid Exhibit Asymmetry In mentioning

confidence: 98%

Molecular and evolutionary strategies of meiotic cheating by selfish centromeres

Akera

Trimm

2018

Preprint

View full text Add to dashboard Cite

Asymmetric division in female meiosis creates selective pressure favoring selfish centromeres that bias their transmission to the egg. This centromere drive can explain the paradoxical rapid evolution of both centromere DNA and centromere-binding proteins despite conserved centromere function. Here, we define a molecular pathway linking expanded centromeres to histone phosphorylation and recruitment of microtubule destabilizing factors in an intraspecific hybrid, leading to detachment of selfish centromeres from spindle microtubules that would direct them to the polar body. We also introduce a second hybrid model, exploiting centromere divergence between species, and show that winning centromeres in one hybrid become losers in the other. Our results indicate that increasing destabilizing activity is a general strategy for drive, but centromeres have evolved distinct strategies to increase that activity. Furthermore, we show that drive depends on slowing meiotic progression, suggesting that a weakened meiotic spindle checkpoint evolved as a mechanism to suppress selfish centromeres.

show abstract

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

Cited by 5 publications

References 29 publications

Distinct classes of lagging chromosome underpin age-related oocyte aneuploidy in mouse

Distinct classes of lagging chromosome underpin age-related oocyte aneuploidy in mouse

Molecular Strategies of Meiotic Cheating by Selfish Centromeres

Molecular and evolutionary strategies of meiotic cheating by selfish centromeres

Contact Info

Product

Resources

About