Cre-LoxP and tamoxifen-induced deletion of ovarian quiescin sulfhydryl oxidase 2 showed disruption of ovulatory activity in mice
Journal
Journal of Ovarian Research
Journal Volume
17
Journal Issue
1
Start Page
Article number 66
ISSN
1757-2215
Date Issued
2024-03-19
Author(s)
Shih-Yun Chen
Tse-En Wang
Wei-Yun Lee
Ya-Yi Yang
Hong-Chun Lai
Fuko Matsuda
Haruhiko Kosek
Sheng-Hsiang Li
Pei-Shiue Tsai
Abstract
Background: Quiescin sulfhydryl oxidase 2 (QSOX2) is a flavin adenine dinucleotide-dependent sulfhydryl oxidase that is known to be involved in protein folding, cell growth regulation, and redox state modification through oxidative activities. Earlier studies demonstrated the tissue and cellular localization of QSOX2 in the male reproductive tract, as well as the highly-regulated mechanism of QSOX2 protein synthesis and expression through the coordinated action of testosterone and epididymal-enriched amino acid, glutamate. However, the presence and the functions of QSOX2 in female reproduction are unknown. In this study, we applied the Cre-loxP gene manipulation system to generate the heterozygous and homozygous Qsox2 knockout mice and examined its effects on ovarian function. Results: We demonstrated that QSOX2 was detected in the follicle-supporting cells (granulosa and cumulus cells) of ovarian follicles of all stages but was absent in the corpus luteum, suggesting its supportive role in folliculogenesis. In comparison with reproductive organogenesis in wild-type mice, there was no difference in testicular and epididymal structure in male Qsox2 knockout; however, Qsox2 knockout disrupted the regular ovulation process in female mice as a drastic decrease in the formation of the corpus luteum was detected, and no pregnancy was achieved when mating males with homozygous Qsox2 knockout females. RNAseq analyses further revealed that Qsox2 knockout altered critical signaling pathways and genes that are responsible for maintaining ovarian functions. Conclusion: Our data demonstrated for the first time that Qsox2 is critical for ovarian function in mice. © The Author(s) 2024.
SDGs
Publisher
Springer Science and Business Media LLC
Type
journal article