Wei Ge

This paper investigates the functional roles of gonadotropins and their receptors in zebrafish reproduction through genetic mutants, revealing three signaling pathways and their impact on fertility and sex differentiation.

The paper identifies the Amh-Bmpr2a-Bmpr1bb signaling pathway in zebrafish and shows its role in gonadal homeostasis, with gonadotropins contributing to gonadal hypertrophy.

This study shows Ybx1 deficiency in zebrafish causes ROS-driven intestinal inflammation, MMP-mediated gut damage, and postnatal lethality, establishing a model for IBD-like disorders.

This study shows Ybx1 promotes zebrafish follicle cell proliferation by suppressing p21, essential for folliculogenesis and female fertility.

This study shows that bmp15 deficiency in zebrafish causes follicle arrest and sex reversal, which can be rescued by inhibin mutation, revealing interactions between bmp15 and the activin-inhibin system in folliculogenesis.

This study shows that loss of Gdf9 in zebrafish causes early follicle arrest and sex reversal, which can be rescued by inhibin mutation, suggesting Gdf9 acts via the activin-inhibin system.

This study identifies lncRNAs involved in redox regulation in ybx1-deficient zebrafish larvae through transcriptome analysis and experimental validation.