Research Paper Volume 13, Issue 1 pp 1001—1016
Conditional deletion of Wntless in granulosa cells causes impaired corpora lutea formation and subfertility
- 1 Institute of Reproductive Medicine, School of Medicine, Nantong University, Nantong 226001, China
- 2 Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Ningxia 751400, China
- 3 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China
Received: August 22, 2020 Accepted: October 9, 2020 Published: December 3, 2020https://doi.org/10.18632/aging.202222
How to Cite
Copyright: © 2020 Cheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
WNT proteins are widely expressed in the murine ovaries. WNTLESS is a regulator essential for all WNTs secretion. However, the complexity and overlapping expression of WNT signaling cascades have prevented researchers from elucidating their function in the ovary. Therefore, to determine the overall effect of WNT on ovarian development, we depleted the Wntless gene in oocytes and granulosa cells. Our results indicated no apparent defect in fertility in oocyte-specific Wntless knockout mice. However, granulosa cell (GC) specific Wntless deletion mice were subfertile and recurred miscarriages. Further analysis found that GC-specific Wntless knockout mice had noticeably smaller corpus luteum (CL) in the ovaries than control mice, which is consistent with a significant reduction in luteal cell marker gene expression and a noticeable increase in apoptotic gene expression. Also, the deletion of Wntless in GCs led to a significant decrease in ovarian HCGR and β-Catenin protein levels. In conclusion, Wntless deficient oocytes had no discernible impact on mouse fertility. In contrast, the loss of Wntless in GCs caused subfertility and impaired CL formation due to reduced LHCGR and β-Catenin protein levels, triggering GC apoptosis.