https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Translational control in mouse folliculogenesis and oocyte development https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13368 Wed 11 Apr 2018 17:48:44 AEST ]]> RNA binding proteins in spermatogenesis: an in depth focus on the Musashi family https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27738 Tue 26 Feb 2019 13:24:45 AEDT ]]> Translational control in germ cell development: a role for the RNA-binding proteins Musashi-1 and Musashi-2 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17662 Sat 24 Mar 2018 07:57:47 AEDT ]]> Developmental expression of Musashi-1 and Musashi-2 RNA-binding proteins during spermatogenesis: analysis of the deleterious effects of dysregulated expression https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20640 Sat 24 Mar 2018 07:55:44 AEDT ]]> Knockout of RNA binding protein MSI2 impairs follicle development in the mouse ovary: characterization of MSI1 and MSI2 during folliculogenesis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27033 Xenopus and is expressed during ovarian development in Drosophila. In mammals Musashi is important for spermatogenesis and male fertility, but its role in the ovary has yet to be characterized. In this study we determined the expression of mammalian Musashi proteins MSI1 and MSI2 during mouse folliculogenesis, and through the use of a MSI2-specific knockout mouse model we identified that MSI2 is essential for normal follicle development. Time-course characterization of MSI1 and MSI2 revealed distinct differences in steady-state mRNA levels and protein expression/localization at important developmental time-points during folliculogenesis. Using a gene-trap mouse model that inactivates Msi2, we observed a significant decrease in ovarian mass, and change in follicle-stage composition due to developmental blocking of antral stage follicles and pre-antral follicle loss through atresia. We also confirmed that hormonally stimulated Msi2-deficient mice produce significantly fewer MII oocytes (60.9% less than controls, p < 0.05). Furthermore, the majority of these oocytes are of poor viability (62.2% non-viable/apoptotic, p < 0.05), which causes a reduction in female fertility evidenced by decreased litter size in Msi2-deficient animals (33.1% reduction to controls, p < 0.05). Our findings indicate that MSI1 and MSI2 display distinct expression profiles during mammalian folliculogenesis and that MSI2 is required for pre-antral follicle development.]]> Fri 13 Sep 2024 12:46:24 AEST ]]>