Search

During the oocyte growth, maturation and zygote development, chromatin structure keeps changing to regulate different nuclear activities. Here, we reported the role of SMC2, a core component of condensin complex, in oocyte and embryo development. Oocyte‐specific conditional knockout of SMC2 caused female infertility. In the absence of SMC2, oocyte meiotic maturation and ovulation occurred normally, but chromosome condensation showed defects and DNA damages were accumulated in oocytes. The pronuclei were abnormally organized and micronuclei were frequently observed in fertilized eggs, their activity was impaired, and embryo development was arrested at the one‐cell stage, suggesting that maternal SMC2 is essential for embryonic development. [ABSTRACT FROM AUTHOR]

Parathyroid hormone‐related protein (PTHrP), the main cause of humoral hypercalcemia in malignancies, promotes cell proliferation and delays terminal cell maturation during embryonic development. Our previous study reported that PTHrP plays important roles in blastocyst formation, pluripotency gene expression, and histone acetylation during mouse preimplantation embryonic development. In this study, we further investigated the mechanism of preimplantation embryonic development regulated by PTHrP. Our results showed that Pthrp depletion decreased both the developmental rate of embryos at the cleavage stage and the cell number of morula‐stage embryos. Pthrp‐depleted embryos had significantly decreased levels of cyclin D1, phospho (p)‐AKT (Thr308) and E2F1. However, Pthrp depletion did not cause significant changes in CDK4, β‐catenin or RUNX2 expression. In addition, our results indicated that Pthrp depletion promoted HDAC4 translocation from the cytoplasm to the nucleus in cleavage‐stage embryos by stimulating the activity of protein phosphatase 2A (PP2A), which resulted in dephosphorylation of HDAC4. Taken together, these results suggest that PTHrP regulates cleavage division progression and blastocyst formation through the AKT/cyclin D1 pathway and that PTHrP modulates histone acetylation patterns through nuclear translocation of HDAC4 via PP2A‐dependent HDAC4 dephosphorylation during preimplantation embryonic development in mice. [ABSTRACT FROM AUTHOR]

In vitro culture of follicles is a promising technology to generate large quantities of mature oocytes and it could offer a novel option of assisted reproductive technologies. Here we described a 2‐dimensional follicular serum‐free culture system with 3‐dimensional effect that can make secondary follicles develop into antral follicles (78.52%), generating developmentally mature oocytes in vitro (66.45%). The oocytes in this serum‐free system completed the first meiosis; spindle assembly and chromosome congression in most oocytes matured from follicular culture were normal. However, these oocytes showed significantly lower activation and embryonic development rates, and their ability to produce Ca2+oscillations was also lower in response to parthenogenetic activation, after which a 2‐cell embryonic developmental block occurred. Oocytes matured from follicular culture displayed increased abnormal mitochondrial distribution and increased reactive oxygen species levels when compared to in vivo matured oocytes. These data are important for understanding the reasons for reduced developmental potential of oocytes matured from follicular culture, and for further improving the cultivation system. [ABSTRACT FROM AUTHOR]

Objectives: In humans, non‐obstructive azoospermia (NOA) is a major cause of male infertility. However, the aetiology of NOA is largely unknown. Previous studies reported that protein CK2β was abundantly and broadly expressed in spermatogenic cells. Here, we investigate whether protein CK2β participates in spermatogenesis. Materials and Methods: In this study, we separated spermatogenic cells using STA‐PUT velocity sedimentation, analysed the expression pattern of protein CK2β by immunoblotting, specifically deleted Ck2β gene in early‐stage spermatogenic cells by crossing Ck2βfl mice with Stra8‐Cre+ mice and validated the knockout efficiency by quantitative RT‐PCR and immunoblotting. The phenotypes of Ck2βfl/Δ;SCre+ mice were studied by immunohistochemistry and immunofluorescence. The molecular mechanisms of male germ cell development arrest were elucidated by immunoblotting and TUNEL assay. Results: Ablation of Ck2β gene triggered excessive germ cell apoptosis, germ cell development arrest, azoospermia and male infertility. Inactivation of Ck2β gene caused distinctly reduced expression of Ck2α′ gene and CK2α′ protein. Conclusions: Ck2β is a vital gene for germ cell survival and male fertility in mice. [ABSTRACT FROM AUTHOR]