ProTAME Arrest in Mammalian Oocytes and Embryos Does Not Require Spindle Assembly Checkpoint Activity

Radonova, Lenka; Svobodova, Tereza; Skultety, Michal; Mrkva, Ondrej; Libichova, Lenka; Stein, Paula; Anger, Martin

doi:10.3390/ijms20184537

Cited by 7 publications

(3 citation statements)

References 27 publications

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“…To explore the cause leading to SAC activation at M I stage, we examined the spindle/chromosome structure which has been previously shown to be involved in the SAC control in oocytes [32]. As expected, we observed that inhibition of CK2 caused a significant increase in the abnormalities of spindle morphology and chromosome alignment in porcine oocytes, indicating that compromised spindle assembly induced the SAC activation at M I stage to block metaphase-anaphase transition and polar body extrusion upon CK2 inhibition.…”

Section: Figsupporting

confidence: 52%

Casein kinase 2 modulates the spindle assembly checkpoint to orchestrate porcine oocyte meiotic progression

ShiYang

Miao

Cui

et al. 2020

J Animal Sci Biotechnol

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Background: CK2 (casein kinase 2) is a serine/threonine-selective protein kinase that has been involved in a variety of cellular processes such as DNA repair, cell cycle control and circadian rhythm regulation. However, its functional roles in oocyte meiosis have not been fully determined. Results: We report that CK2 is essential for porcine oocyte meiotic maturation by regulating spindle assembly checkpoint (SAC). Immunostaining and immunoblotting analysis showed that CK2 was constantly expressed and located on the chromosomes during the entire oocyte meiotic maturation. Inhibition of CK2 activity by its selective inhibitor CX-4945 impaired the first polar body extrusion and arrested oocytes at M I stage, accompanied by the presence of BubR1 at kinetochores, indicative of activated SAC. In addition, we found that spindle/chromosome structure was disrupted in CK2-inhibited oocytes due to the weakened microtubule stability, which is a major cause resulting in the activation of SAC. Last, we found that the level DNA damage as assessed by γH2A.X staining was considerably elevated when CK2 was inhibited, suggesting that DNA damage might be another critical factor leading to the SAC activation and meiotic failure of oocytes. Conclusions: Our findings demonstrate that CK2 promotes the porcine oocyte maturation by ensuring normal spindle assembly and DNA damage repair.

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Section: Figsupporting

confidence: 52%

Casein kinase 2 modulates the spindle assembly checkpoint to orchestrate porcine oocyte meiotic progression

ShiYang

Miao

Cui

et al. 2020

J Animal Sci Biotechnol

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“…Regarding the expression of SAC core components in the embryo, it was shown that Mad2, Bub3, and BubR1 are detectable in zygotes and their depletion by RNAi caused the acceleration of the first mitosis, insensitivity to nocodazole, and chromosome segregation defects [137]. Another study, however, showed that in zygotes and two-cell embryos, the interaction of overexpressed Mad1 with kinetochores is only brief and that the protein quickly disengages from the chromosomes after NEBD [138]. Recently published results showed that mouse morulas are insensitive to chromosome segregation defects, and the misaligned chromosomes do not delay the onset of anaphase [139].…”

Section: Control Of Chromosome Segregation During Early Embryonic Dev...mentioning

confidence: 99%

Chromosome Division in Early Embryos—Is Everything under Control? And Is the Cell Size Important?

Horakova,

Konecna,

Anger

2024

IJMS

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Chromosome segregation in female germ cells and early embryonic blastomeres is known to be highly prone to errors. The resulting aneuploidy is therefore the most frequent cause of termination of early development and embryo loss in mammals. And in specific cases, when the aneuploidy is actually compatible with embryonic and fetal development, it leads to severe developmental disorders. The main surveillance mechanism, which is essential for the fidelity of chromosome segregation, is the Spindle Assembly Checkpoint (SAC). And although all eukaryotic cells carry genes required for SAC, it is not clear whether this pathway is active in all cell types, including blastomeres of early embryos. In this review, we will summarize and discuss the recent progress in our understanding of the mechanisms controlling chromosome segregation and how they might work in embryos and mammalian embryos in particular. Our conclusion from the current literature is that the early mammalian embryos show limited capabilities to react to chromosome segregation defects, which might, at least partially, explain the widespread problem of aneuploidy during the early development in mammals.

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“…The activation of APC/C in the medium term is controlled by a checkpoint mechanism called Spindle Assembly Checkpoint (SAC) [11], which monitors the correct connection of all moving shafts to the spindle, bipolar spindle is the key to cell division in order to guide the correct separation of chromosomes [12].…”

Section: Advanced Maternal Age and Chromosomal Abnormalitiesmentioning

confidence: 99%

The Risk of Advanced Maternal Age: Causes and Overview

Liu¹,

Lü²,

Zhang³

et al. 2020

J Gynecol Res Obstet

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Since 1980, the progress of modern society has greatly affected the fertility of women. In recent years, there has been an increase in the number of (AMA) among non-pregnant and older mothers-that is, women with childbearing age greater than or equal to 35 years of age, especially at the senior level in both developed and developing countries. Over the past few decades, the age structure of the world's reproductive population has changed dramatically. In China, the age structure of childbearing population keeps changing. The fertility rate of women aged 35 to 39 was 8.65% in 2004 and 17.04% ten years later. By 2016, the rate of late pregnancy was about 31% [1-3]. In Europe, the probability of chromosomal abnormalities increases with the age of the mother. In 2016, the Chinese government liberalized the "two-child policy" and gradually replaced the "one-child policy". The new policy encourages couples to have two or more children, which may lead to more pregnant woman [4]. AMA has gradually become an important social and clinical issue. At present, the proportion of women who have delayed their childbearing age to 35 years old has increased signifi cantly, especially in Western countries. At present, the delay in childbearing age may be related to a variety of factors, such as female education level and career goals, effective contraceptive strategies, lack of support for parental social incentives, and a widely disseminated misconception that assisted reproductive technology can compensate for infertility that naturally decreases with age [3]. The older the parents are pregnant, the higher the risk of illness in their offspring [5]. There is a large body of research and data confi rming a negative correlation between maternal age and child health at birth. The live birth rate of AMA is lower than that of young women conceived through natural or assisted reproductive technology. To some extent, the decrease of fertility is due to the increase of ovary aneuploidy, which leads to the decrease of embryo quality and abortion [6,7]. However, the biochemical mechanism of aging affecting ovary and embryo quality remains to be clarifi ed. The reasons for the decline of ovarian reserve in AMA are considered to be energy production disorders, cell cycle checkpoints, and meiotic

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ProTAME Arrest in Mammalian Oocytes and Embryos Does Not Require Spindle Assembly Checkpoint Activity

Cited by 7 publications

References 27 publications

Casein kinase 2 modulates the spindle assembly checkpoint to orchestrate porcine oocyte meiotic progression

Casein kinase 2 modulates the spindle assembly checkpoint to orchestrate porcine oocyte meiotic progression

Chromosome Division in Early Embryos—Is Everything under Control? And Is the Cell Size Important?

The Risk of Advanced Maternal Age: Causes and Overview

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