Abstract
Premature ovarian insufficiency (POI) refers to severe decline of ovary function in females which usually leads to infertility. It has been reported that the TMEM150B gene is mostly associated with age at natural menopause, early menopause and POI, but its role in female reproduction remains unknown. In this study, we found Tmem150b was highly expressed in mouse oocytes, but its deletion had no obvious effect on meiotic maturation of oocytes indicated by first polar body emission and spindle morphology. There were also no obvious differences in follicle development and corpus luteum formation between knockout and wild type mice. Finally, knockout of Tmem150b did not affect female fertility and sexual hormone levels. In summary, our results suggest that TMEM150B is not essential for female fertility in mice.
Highlights
Premature ovarian insufficiency (POI) refers to severe decline of ovary function in females which usually leads to infertility
Premature ovarian insufficiency (POI) causes fertility decline in women which is characterized by defect of ovarian function with serum follicle-stimulating hormone (FSH) level over 25 IU/L before the age of 40 y ears[1,2]
Causative genes associated with POI have been identified, such as genes associated with follicular development (FIGLA, FSHR, NOBOX, GDF9 and BMP15), and genes related to meiosis and DNA repair (STAG3, HFM1, MCM8, MCM9 and MSH5)[5]
Summary
Premature ovarian insufficiency (POI) refers to severe decline of ovary function in females which usually leads to infertility. It has been reported that the TMEM150B gene is mostly associated with age at natural menopause, early menopause and POI, but its role in female reproduction remains unknown. Premature ovarian insufficiency (POI) causes fertility decline in women which is characterized by defect of ovarian function with serum follicle-stimulating hormone (FSH) level over 25 IU/L before the age of 40 y ears[1,2]. Several genes related to these loci, such as MCM8, MSH5 and SYCP2L, have been identified[7,8] Their knockout mice exhibit infertility, ovarian dysgenesis or premature insufficiency[9,10,11], and mutations in these genes were found in POI patients and the causality was confirmed by functional studies[12,13,14,15]. We generated the Tmem150b knockout mouse model to explore the potential role of TMEM150B in female reproduction
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