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Project description:Oocyte maturation defects are one contributing factor in unexplained female infertility. Failure of some oocytes to undergo germinal vesicle breakdown or progress to second meiotic metaphase in response to an ovulatory stimulus can limit the number of high quality oocytes available for assisted reproduction. Understanding the molecular mechanisms that underlie oocyte maturation failure may lead to novel methods for increasing the number of high quality oocytes available for assisted reproduction, as well as providing new insight into the basic biology of oocyte maturation. Using RNA sequencing, we compared the transcriptome of rhesus monkey oocytes that failed to mature (FTM) in response to an ovulatory stimulus in vivo to normal germinal vesicle and metaphase II stage oocytes.
2018-09-06 | GSE112533 | GEO
Project description:Transcriptome analysis of rhesus monkey germinal vesicle, failed-to-mature oocytes and MII oocytes
| PRJNA448148 | ENA
Project description:Transcriptome analysis of rhesus monkey germinal vesicle and failed-to-mature oocytes
| PRJNA448151 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-09-09 | GSE112537 | GEO
Project description:Oocyte maturation defects are one contributing factor in unexplained female infertility. Failure of some oocytes to undergo germinal vesicle breakdown or progress to second meiotic metaphase in response to an ovulatory stimulus can limit the number of high quality oocytes available for assisted reproduction. Understanding the molecular mechanisms that underlie oocyte maturation failure may lead to novel methods for increasing the number of high quality oocytes available for assisted reproduction, as well as providing new insight into the basic biology of oocyte maturation. Using RNA sequencing, we compared the transcriptome of rhesus monkey oocytes that failed to mature (FTM) in response to an ovulatory stimulus in vivo to normal germinal vesicle and metaphase II stage oocytes.
2018-09-06 | GSE112534 | GEO
Project description:Transcriptome analysis of rhesus monkey MII oocytes
| PRJNA448150 | ENA
Project description:Transcriptome analysis of rhesus monkey MII oocytes and embryos
| PRJNA448147 | ENA
Project description:BackgroundHigh-temperature requirement protease A2 (HtrA2/Omi) is a mitochondrial chaperone that is highly conserved from bacteria to humans. It plays an important role in mitochondrial homeostasis and apoptosis. In this study, we investigated the role of HtrA2 in mouse oocyte maturation.MethodsThe role of HtrA2 in mouse oocyte maturation was investigated by employing knockdown (KD) or overexpression (OE) of HtrA2 in young or old germinal vesicle (GV) oocytes. We employed immunoblotting, immunostaining, fluorescent intensity quantification to test the HtrA2 knockdown on the GV oocyte maturation progression, spindle assembly checkpoint, mitochondrial distribution, spindle organization, chromosome alignment, actin polymerization, DNA damage and chromosome numbers and acetylated tubulin levels.ResultsWe observed a significant reduction in HtrA2 protein levels in aging germinal vesicle (GV) oocytes. Young oocytes with low levels of HtrA2 due to siRNA knockdown were unable to complete meiosis and were partially blocked at metaphase I (MI). They also displayed significantly more BubR1 on kinetochores, indicating that the spindle assembly checkpoint was triggered at MI. Extrusion of the first polar body (Pb1) was significantly less frequent and oocytes with large polar bodies were observed when HtrA2 was depleted. In addition, HtrA2 knockdown induced meiotic spindle/chromosome disorganization, leading to aneuploidy at metaphase II (MII), possibly due to the elevated level of acetylated tubulin. Importantly, overexpression of HtrA2 partially rescued spindle/chromosome disorganization and reduced the rate of aneuploidy in aging GV oocytes.ConclusionsCollectively, our data suggest that HtrA2 is a key regulator of oocyte maturation, and its deficiency with age appears to contribute to reproduction failure in females.
| S-EPMC9764539 | biostudies-literature
Project description:OBJECTIVE:To evaluate the effect of cytoplasm transfer from mature oocytes to germinal vesicle(GV)s on promoting the maturation of cytoplasm of GV at the mRNA level. MATERIALS AND METHODS:Sixty six in vitro fertilization (IVF) operations between June 2012 and November 2013 were included in this study. Totally 120 GVs were obtained. Normal GVs were categorized into 3 groups (n = 40) randomly: the first comprised oocytes that did not receive the cytoplasm of mature oocytes; the second group comprised oocytes that did not receive the cytoplasm of mature oocytes but were incubated for 24 h; and the third group comprised oocytes that received 10-15% the cytoplasm of mature oocytes and were then incubated for 24 h. Each group was separately analyzed by quantitative polymerase chain reaction (qPCR) and the expression levels of selected genes were assessed. RESULTS:The expression levels of genes involved in the cytoplasmic maturity, and energy-producing mitochondria were significantly higher in the pooled oocytes of 2(nd) control group than those of the 1(st) control and intervention groups (p < 0.001). The genes involved in the meiosis, spindle check point, DNA repairing and cell cycle checkpoint did not have any expression in the 1(st) and intervention groups; however, these genes were expressed in the 2(nd) group, significantly. In the 2(nd) group, the highest expression level was observed for genes involved in the DNA repairing and cell cycle checkpoint. In the intervention group, none of the genes were expressed except for energy-producing mitochondria gene; even in this case, the expression level of this gene in this group of oocytes was significantly lower than that in other groups (p < 0.001). After 24 h meiosis assumption was significantly higher in the third group than in the second group (95% vs. 68%, p < 0.001). CONCLUSION:The cytoplasm transfer technique is not effective in cytoplasmic maturity of the recipient GV oocytes. In contrast, 24-hr in-vitro culture is associated with increased expression of studied genes in GVs.
| S-EPMC5026671 | biostudies-literature
Project description:Prior to maturation, mouse oocytes are arrested at the germinal vesicle (GV) stage during which they experience constitutive calcium (Ca2+) influx and spontaneous Ca2+ oscillations. The oscillations cease during maturation but Ca2+ influx continues, as the oocytes' internal stores attain maximal content at the culmination of maturation, the metaphase II stage. The identity of the channel(s) that underlie this Ca2+ influx has not been completely determined. GV and matured oocytes are known to express three Ca2+ channels, CaV3.2, TRPV3 and TRPM7, but females null for each of these channels are fertile and their oocytes display minor modifications in Ca2+ homeostasis, suggesting a complex regulation of Ca2+ influx. To define the contribution of these channels at the GV stage, we used different divalent cations, pharmacological inhibitors and genetic models. We found that the three channels are active at this stage. CaV3.2 and TRPM7 channels contributed the majority of Ca2+ influx, as inhibitors and oocytes from homologous knockout (KO) lines showed severely reduced Ca2+ entry. Sr2+ influx was promoted by CaV3.2 channels, as Sr2+ oscillations were negligible in CaV3.2-KO oocytes but robust in control and Trpv3-KO GV oocytes. Mn2+ entry relied on expression of CaV3.2 and TRPM7 channels, but Ni2+ entry depended on the latter. CaV3.2 and TRPV3 channels combined to fill the Ca2+ stores, although CaV3.2 was the most impactful. Studies with pharmacological inhibitors effectively blocked the influx of divalent cations, but displayed off-target effects, and occasionally agonist-like properties. In conclusion, GV oocytes express channels mediating Ca2+ and other divalent cation influx that are pivotal for fertilization and early development. These channels may serve as targets for intervention to improve the success of assisted reproductive technologies.
| S-EPMC7153984 | biostudies-literature