Obox1 deficiency induceds subfertility in female mice
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ABSTRACT:
PROVIDER: PRJNA855632 | ENA |
REPOSITORIES: ENA
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Project description:Obox1 was considered to be a maternal factor participates in oogenesis and follicle development, but its function remains largely undefined. In this study, we demonstrated that Obox1-null female mice displayed subfertility as evidenced by decreased litter size. Obox1 deficiency resulted in less oocytes production. The levels of female sex hormones and gonadotropins, especially luteinizing hormone (LH), were significantly decreased both in ovaries and serum at diestrus. Further studies showed that Obox1-null ovaries were hypo-reactive to LH. There are still more unruptured follicles in the ovaries after superovulation in Obox1-null ovaries. The number of corpus luteum (CL) and serum concentration of progesterone (P4) reduced, and the steroidogenesis-related genes were aberrant in Obox1-null mice. In conclusion, Obox1 deficiency impaired ovulation and luteinization and led to female subfertility.
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Project description:Research has shown that Taf4b-deficient female mice display excessive perinatal germ cell death, delayed germ cell cyst breakdown, and increased chromosome asynapsis. Therefore, we hypothesized that TAF4b, as part of TFIID, regulates oogenesis and meiotic gene programs. However, the transcriptomic effects of Taf4b-deficiency and how this may lead to the infertility we observe in mice has not yet been studied. Therefore, we performed RNA-seq to examine gene expression changes in E16.5 female Taf4b-heterozygous and Taf4b-deficient germ cells
2022-01-26 | GSE174365 | GEO
Project description:Research has shown that Taf4b-deficient female mice display excessive perinatal germ cell death, delayed germ cell cyst breakdown, and increased chromosome asynapsis. Therefore, we hypothesized that TAF4b, as part of TFIID, regulates oogenesis and meiotic gene programs. However, the transcriptomic effects of Taf4b-deficiency and how this may lead to the infertility we observe in mice has not yet been studied. Therefore, we performed RNA-seq to examine gene expression changes in E14.5 female Taf4b-wildtype, Taf4b-heterozygous, and Taf4b-deficient germ cells
2022-01-26 | GSE174364 | GEO
Project description:After fertilization the developing mammalian embryo migrates through the oviduct before it implants in the uterus. In order to prevent tubal pregnancy or failed implantation, development and migration of the embryo has to be tightly coordinated1. The precise molecular basis for the regulation of this maternal-embryonic interaction is largely unknown. Here we show that the Wilms tumor suppressor protein Wt1 is a critical regulator of the interaction between the maternal environment and the early embryo. Our results indicate that subfertility in Wt1ko/+ females is a maternal effect caused by the Wt1-dependent de-regulation of Prss29, encoding a serine protease. Notably, blocking Prss29 activity was sufficient to rescue subfertility in Wt1ko/+ female mice indicating Prss29 as a critical factor in female fertility. Furthermore, we have identified a missense mutation in a patient with idiopathic infertility leading to an amino acid exchange within the zinc finger domain of WT1 and resulting in reduced DNA binding. We demonstrate that Wt1 represses expression of Prss29 and that its de-repression and precocious expression in the oviduct interferes with pre-implantation development. Our study reveals a novel role for Wt1 in early mammalian development and identifies proteases as critical mediators of the maternal-embryonic crosstalk. We believe that our data regarding the importance of a proteostatic environment in the oviduct are also relevant for female fertility in humans. We anticipate that our findings will form the basis for the identification of further causes of idiopathic infertility.
2017-04-04 | PXD003283 | Pride
Project description:NLRP14 deficiency contributes to female infertility and early embryo arrest
| PRJNA979177 | ENA