Reduced Vitellogenesis and Female Fertility in Gper Knockout Zebrafish
- Wu, X.J., Williams, M.J., Kew, K.A., Converse, A., Thomas, P., Zhu, Y.
- Frontiers in endocrinology 12: 637691 (Journal)
- Registered Authors
- Thomas, Peter, Wu, Xi-Jun, Zhu, Yong
- G-protein coupled estrogen receptor (Gper), epidermal growth factor receptor (Egfr), oocyte growth, reduced fertility, vitellogenin
- MeSH Terms
- Cell Membrane/metabolism
- ErbB Receptors/metabolism
- Ovarian Follicle/metabolism
- Receptors, Estrogen/metabolism
- Receptors, G-Protein-Coupled/genetics*
- Receptors, G-Protein-Coupled/metabolism
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- 33790865 Full text @ Front Endocrinol (Lausanne)
Wu, X.J., Williams, M.J., Kew, K.A., Converse, A., Thomas, P., Zhu, Y. (2021) Reduced Vitellogenesis and Female Fertility in Gper Knockout Zebrafish. Frontiers in endocrinology. 12:637691.
The role G-protein coupled estrogen receptor (GPER) plays in vertebrate reproduction remains controversial. To investigate GPER's reproductive role, we generated a gper zebrafish mutant line (gper-/- ) using TALENs. Gper mutant females exhibited reduced fertility with a 40.85% decrease in embryo production which was associated with a significant decrease in the number of Stage V (730-750 μm) ovulated oocytes. Correspondingly, the number of early vitellogenic follicles (Stage III, 400-450 µm) in gper-/- ovaries was greater than that in wildtypes (wt), suggesting that subsequent follicle development was retarded in the gper-/- fish. Moreover, plasma vitellogenin levels were decreased in gper-/- females, and epidermal growth factor receptor (Egfr) expression was lower in Stage III vitellogenic oocytes than in wt counterparts. However, hepatic nuclear estrogen receptor levels were not altered, and estrogen levels were elevated in ovarian follicles. These results suggest that Gper is involved in the control of ovarian follicle development via regulation of vitellogenesis and Egfr expression in zebrafish.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes