https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34201 In vivo genetic cell lineage tracing showed that secretory cells not only self-renew, but also give rise to ciliated cells. Analysis of a Wnt reporter mouse model and various Wnt target genes showed that the Wnt signaling pathway is involved in oviductal epithelial homoeostasis. By developing two triple-transgenic mouse models, we showed that Wnt/ ß-catenin signaling is essential for self-renewal as well as the differentiation of secretory cells. In summary, our results provide mechanistic insight into oviductal epithelial homoeostasis.]]> Wed 19 Jan 2022 15:14:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6546 Wed 11 Apr 2018 16:15:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21342 Wed 11 Apr 2018 12:17:52 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24259 Wed 11 Apr 2018 11:39:29 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6548 Wed 11 Apr 2018 10:37:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7337 Sat 24 Mar 2018 08:35:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11246 Cdh1) activity, which ubiquitylates and so targets cyclin B1 for degradation. Thus, APC^Cdh1 activity prevents precocious meiotic entry by promoting cyclin B1 degradation. However, it remains unresolved how cyclin B1 levels are suppressed sufficiently to maintain arrest but not so low that they make oocytes hormonally insensitive. Here, we examined spatial control of this process by determining the intracellular location of the proteins involved and using nuclear-targeted cyclin B1. We found that raising nuclear cyclin B1 concentrations, an event normally observed in the minutes before nuclear envelope breakdown, was a very effective method of inducing the G2/M transition. Oocytes expressed only the α-isoform of Cdh1, which was predominantly nuclear, as were Cdc27 and Psmd11, core components of the APC and the 26S proteasome, respectively. Furthermore, APC^Cdh1 activity appeared higher in the nucleus, as nuclear-targeted cyclin B1 was degraded at twice the rate of wild-type cyclin B1. We propose a simple spatial model of G2 arrest in which nuclear APC^Cdh1-proteasomal activity guards against any cyclin B1 accumulation mediated by nuclear import.]]> Sat 24 Mar 2018 08:10:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21158 FZR1 activity in the male germline led to both a mitotic and a meiotic testicular defect resulting in infertility due to the absence of mature spermatozoa. Spermatogonia in the prepubertal testes of such mice had abnormal proliferation and delayed entry into meiosis. Although early recombination events were initiated, male germ cells failed to progress beyond zygotene and underwent apoptosis. Loss of APC/C^FZR1 activity was associated with raised cyclin B1 levels, suggesting that CDK1 may trigger apoptosis. By contrast, female FZR1Δ mice were subfertile, with premature onset of ovarian failure by 5 months of age. Germ cell loss occurred embryonically in the ovary, around the time of the zygotene-pachytene transition, similar to that observed in males. In addition, the transition of primordial follicles into the growing follicle pool in the neonatal ovary was abnormal, such that the primordial follicles were prematurely depleted. We conclude that APC/C^FZR1 is an essential regulator of spermatogonial proliferation and early meiotic prophase I in both male and female germ cells and is therefore important in establishing the reproductive health of adult male and female mammals.]]> Sat 24 Mar 2018 08:00:18 AEDT ]]>