SummarySister chromatid cohesion mediated by the cohesin complex is essential for chromosome segregation in mitosis and meiosis [1]. Rec8-containing cohesin, bound to Smc3/Smc1α or Smc3/Smc1β, maintains bivalent cohesion in mammalian meiosis [2, 3, 4, 5, 6]. In females, meiotic DNA replication and recombination occur in fetal oocytes. After birth, oocytes arrest at the prolonged dictyate stage until recruited to grow into mature oocytes that divide at ovulation. How cohesion is maintained in arrested oocytes remains a pivotal question relevant to maternal age-related aneuploidy. Hypothetically, cohesin turnover regenerates cohesion in oocytes. Evidence for post-replicative cohesion establishment mechanism exists, in yeast and invertebrates [7, 8]. In mouse fetal oocytes, cohesin loading factor Nipbl/Scc2 localizes to chromosome axes during recombination [9, 10]. Alternatively, cohesion is maintained without turnover. Consistent with this, cohesion maintenance does not require Smc1β transcription, but unlike Rec8, Smc1β is not required for establishing bivalent cohesion [11, 12]. Rec8 maintains cohesion without turnover during weeks of oocyte growth [3]. Whether the same applies to months or decades of arrest is unknown. Here, we test whether Rec8 activated in arrested mouse oocytes builds cohesion revealed by TEV cleavage and live-cell imaging. Rec8 establishes cohesion when activated during DNA replication in fetal oocytes using tamoxifen-inducible Cre. In contrast, no new cohesion is detected when Rec8 is activated in arrested oocytes by tamoxifen despite cohesin synthesis. We conclude that cohesion established in fetal oocytes is maintained for months without detectable turnover in dictyate-arrested oocytes. This implies that women’s fertility depends on the longevity of cohesin proteins that established cohesion in utero.

Problem Cytokines, mediators of the immune response, are involved in the regulation of female reproductive processes during the estrous cycle and pregnancy. The present study aimed to investigate the effect of selected peroxisome proliferator‐activated receptor gamma (PPARγ) ligands on the expression of nuclear factor kappa B (NF‐κB) and selected cytokines, such as interleukin (IL)‐1β, ‐4, ‐6, ‐8, ‐10, and the leukemia inhibitory factor, in the porcine endometrium on days 10‐12 and 14‐16 of the estrous cycle (mid‐ and late luteal phase, respectively) or pregnancy (maternal recognition of pregnancy and beginning of implantation, respectively). Method of study Endometrial slices were incubated in vitro in the presence of PPARγ agonists, 15‐deoxy‐Δ12, 14‐prostaglandin J2 or rosiglitazone, and PPARγ antagonist T0070907. mRNA and protein levels in tissues were determined by real‐time PCR and Western blot. Results On days 10‐12 of the estrous cycle and days 14‐16 of pregnancy, PPARγ ligands enhanced the expression of NF‐κB, mRNA cytokines, and/or proteins. During the late luteal phase of the estrous cycle (days 14‐16) and maternal recognition of pregnancy (days 10‐12), PPARγ ligands inhibited the expression of NF‐κB, and they differentially affected the expression of mRNA and proteins of cytokines. Conclusion Our results indicate that PPARγ is engaged in the endometrial synthesis of NF‐κB and selected cytokines in pigs. The influence of PPARγ ligands on the tested components of the immune system varied subject to the physiological status of females, and it could be associated with differences in endometrial receptivity.

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