ArticleBiomolecules2015
Knockout of RNA Binding Protein MSI2 Impairs Follicle Development in the Mouse Ovary: Characterization of MSI1 and MSI2 during Folliculogenesis.
Article in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- MSI2 in the dentate gyrus and ovary regulates the reproductive endocrine homeostasis of female mice.Communications biology · 2025Article
- In Vitro Fertilization Accelerates Female Reproductive Aging Through Early Ovarian Failure.bioRxiv : the preprint server for biology · 2025Article
- Identification of FSH-regulated and estrous stage-specific transcriptional networks in mouse ovaries.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Small-molecule Ro-08-2750 interacts with many RNA-binding proteins and elicits MUSASHI2-independent phenotypes.RNA (New York, N.Y.) · 2023Article
- MiMIC analysis reveals an isoform specific role for Drosophila Musashi in follicle stem cell maintenance and escort cell function.Cell death discovery · 2022Article
- Potential Role of Musashi-2 RNA-Binding Protein in Cancer EMT.OncoTargets and therapy · 2021Review
- Review
- A combinatorial code for mRNA 3'-UTR-mediated translational control in the mouse oocyte.Nucleic acids research · 2019Article
- Musashi RNA-Binding Proteins as Cancer Drivers and Novel Therapeutic Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Characterizing the mechanisms underlying follicle development in the ovary is crucial to understanding female fertility and is an area of increasing research interest. The RNA binding protein Musashi is essential for post-transcriptional regulation of oocyte maturation in 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.
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