LAUSR

Abstract 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. Summary Sentence The impact of maternal aging on Ca2+ homeostasis in fertilized mouse oocytes varies depending on the genetic origin of females. Graphical Abstract