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Published on: October 13, 2018
Dicer is required for female reproductive tract development and fertility in the mouse
Gabriel Gonzalez1, Richard R Behringer
1Department of Genetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Abstract:
Dicer encodes a riboendonuclease required for microRNA biosynthesis. Dicer was inactivated in Müllerian duct mesenchyme-derived tissues of the reproductive tract of the mouse, using an Amhr2-Cre allele. Although Amhr2-Cre; Dicer conditional mutant males appeared normal and were fertile, mutant females were infertile. In adult mutant females, there was a reduction in the size of the oviducts and uterine horns. The oviducts were less coiled compared to controls and cysts formed at the isthmus near the uterotubal junction. Unfertilized, degenerate oocytes were commonly found within these cysts, indicating a defect in embryo transit. Beads transferred into the mutant oviduct failed to migrate into the uterus. In addition, blastocysts transferred directly into the mutant uterus did not result in pregnancy. Histological analysis demonstrated that the mutant uterus contained less glandular tissue and often the few glands that remained were found within the myometrium, an abnormal condition known as adenomyosis. In adult mutants, there was ectopic expression of Wnt4 and Wnt5a in the luminal epithelium (LE) and glandular epithelium (GE) of the uterus, and Wnt11 was ectopically expressed in GE. These results demonstrate that Dicer is necessary for postnatal differentiation of Müllerian duct mesenchyme-derived tissues of the female reproductive tract, suggesting that microRNAs are important regulators of female reproductive tract development and fertility.
Insights
Dicer is essential for female reproductive tract development. Inactivating Dicer in mice caused infertility, oviduct defects, and uterine adenomyosis, highlighting microRNAs' role in fertility.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are small non-coding RNAs crucial for gene regulation.
- Dicer is a key enzyme in miRNA biosynthesis, essential for processing precursor miRNAs into mature miRNAs.
- The role of Dicer and miRNAs in the postnatal development and function of the female reproductive tract remains incompletely understood.
Purpose of the Study:
- To investigate the function of Dicer in the postnatal development and fertility of the mouse female reproductive tract.
- To determine the specific defects caused by Dicer inactivation in Müllerian duct mesenchyme-derived tissues.
- To explore the downstream molecular mechanisms, including Wnt signaling, affected by Dicer deficiency.
Main Methods:
- Conditional inactivation of the Dicer gene in Müllerian duct mesenchyme-derived tissues using the Amhr2-Cre driver line.
- Phenotypic analysis of reproductive organs in Dicer conditional mutant mice (males and females).
- Fertility assessment, embryo and bead transfer experiments, histological analysis, and gene expression studies (Wnt4, Wnt5a, Wnt11).
Main Results:
- Conditional Dicer inactivation led to infertility in female mice, while males remained fertile.
- Mutant females exhibited reduced oviducts and uterine horns, oviductal cysts, and impaired embryo transport.
- Histological analysis revealed reduced glandular tissue and adenomyosis in the mutant uterus, with ectopic Wnt signaling.
- Ectopic expression of Wnt4, Wnt5a, and Wnt11 was observed in the uterine epithelium of mutant females.
Conclusions:
- Dicer is indispensable for the postnatal differentiation and function of the female reproductive tract derived from Müllerian duct mesenchyme.
- MicroRNAs regulated by Dicer play critical roles in female fertility, oviduct development, and uterine homeostasis.
- Disruption of Dicer function leads to reproductive abnormalities, including infertility and adenomyosis, mediated in part by aberrant Wnt signaling.
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