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Age-related alterations in fertilization-induced Ca2+ oscillations depend on the genetic background of mouse oocytes.
Biology of Reproduction ( IF 3.6 ) Pub Date : 2020-08-06 , DOI: 10.1093/biolre/ioaa139
Katarzyna Czajkowska 1 , Agnieszka Walewska 1 , Takao Ishikawa 2 , Katarzyna Szczepańska 1 , Anna Ajduk 1
Affiliation  

Maternal aging affects various aspects of oocytes’ physiology, including the functionality of their nuclear apparatus and mitochondria. In the present paper, we wished to investigate whether advanced reproductive age impacts oocytes’ ability to generate proper Ca2+ oscillations in response to monospermic fertilization. We examined three different mouse strains/crosses: inbred C57BL/6Tar, outbred Tar:SWISS, and hybrid F1 (C57BL/6Tar × CBA/Tar). The females were either 2–4 months old (young) or 13–16 months old (aged). We observed that the Ca2+ oscillatory pattern is altered in a strain-dependent manner and changes were more profound in aged C57BL/6Tar and F1 than in aged Tar:SWISS oocytes. We also showed that maternal aging differently affects the size of Ca2+ store and expression of Itpr1, Atp2a2, Erp44, and Pdia3 genes involved in Ca2+ homeostasis in oocytes of C57BL/6Tar, Tar:SWISS, and F1 genetic background, which may explain partially the differences in the extent of age-dependent changes in the Ca2+ oscillations in those oocytes. Maternal aging did not have any visible impact on the distribution of the ER cisterns in oocytes of all three genetic types. Finally, we showed that maternal aging alters the timing of the first embryonic interphase onset and that this timing correlates in C57BL/6Tar and Tar:SWISS oocytes with the frequency of fertilization-induced Ca2+ oscillations. Our results indicate that extreme caution is required when conclusions about oocyte/embryo physiological response to aging are made and complement an increasing amount of evidence that mammalian (including human) susceptibility to aging differs greatly depending on the genetic background of the individual.

中文翻译:

受精诱导的 Ca2+ 振荡的年龄相关改变取决于小鼠卵母细胞的遗传背景。

母体衰老会影响卵母细胞生理的各个方面,包括其核器和线粒体的功能。在本文中,我们希望调查高龄生育期是否会影响卵母细胞响应单精子受精而产生适当 Ca 2+振荡的能力。我们检查了三种不同的小鼠品系/杂交:近交 C57BL/6Tar、远交焦油:SWISS 和杂交 F1(C57BL/6Tar × CBA/Tar)。雌性是 2-4 个月大(年轻)或 13-16 个月大(老)。我们观察到 Ca 2+振荡模式以依赖应变的方式发生改变,并且在老化的 C57BL/6Tar 和 F1 中的变化比在老化的 Tar:SWISS 卵母细胞中更显着。我们还表明,母亲的衰老对 Ca 2+的大小有不同的影响在 C57BL/6Tar、Tar:SWISS 和 F1 遗传背景的卵母细胞中参与 Ca 2+稳态的Itpr1Atp2a2Erp44Pdia3基因的储存和表达,这可能部分解释了年龄依赖性变化程度的差异这些卵母细胞中的 Ca 2+振荡。母体衰老对所有三种遗传类型的卵母细胞中 ER 池的分布没有任何可见的影响。最后,我们发现母体衰老改变了第一个胚胎间期开始的时间,并且该时间与 C57BL/6Tar 和 Tar:SWISS 卵母细胞与受精诱导的 Ca 2+频率相关振荡。我们的研究结果表明,当得出关于卵母细胞/胚胎对衰老的生理反应的结论时,需要极其谨慎,并补充越来越多的证据,即哺乳动物(包括人类)对衰老的敏感性因个体的遗传背景而异。
更新日期:2020-08-06
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