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Fgf22 and Fgfr2b are required for neurogenesis and gliogenesis in the zebrafish forebrain.
Miyake, Ayumi; Ohmori, Takatoshi; Murakawa, Yuka.
Affiliation
  • Miyake A; Department of Genetic Biochemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Kyoto, 606-8501, Japan; Department of Molecular Biology, School of Pharmaceutical Sciences, Wakayama Medical University, 25-1, Shichibancho, Wakayama, 640-8156, Japan. Electronic address: miyakea@wakayama-med.ac.jp.
  • Ohmori T; Department of Genetic Biochemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Kyoto, 606-8501, Japan; Department of Molecular Biology, School of Pharmaceutical Sciences, Wakayama Medical University, 25-1, Shichibancho, Wakayama, 640-8156, Japan.
  • Murakawa Y; Department of Genetic Biochemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Kyoto, 606-8501, Japan.
Biochem Biophys Res Commun ; 681: 212-217, 2023 11 12.
Article in En | MEDLINE | ID: mdl-37783119
ABSTRACT
Fibroblast growth factors (Fgfs) play crucial roles in various developmental processes including brain development. We previously identified Fgf22 in zebrafish and found that fgf22 is involved in midbrain patterning during embryogenesis. Here, we investigated the role of Fgf22 in the formation of the zebrafish forebrain. We found that fgf22 was essential for determining the ventral properties of the telencephalon and diencephalon but not for cell proliferation. In addition, the knockdown of fgf22 inhibited the generation of glutamatergic neurons, γ-aminobutyric acid (GABA)ergic interneurons and astrocytes. Recently, Fgf signaling has received much attention because of its importance in the pathogenesis of multiple sclerosis, in which oligodendrocytes and myelin are destroyed. However, the effects of each Fgf on oligodendrocytes remain largely unknown. Therefore, we also investigated the role of Fgf22 in oligodendrocyte development and explored whether there is a difference between Fgf22 and other Fgfs. Knockdown of fgf22 promoted the generation of oligodendrocytes. Conversely, overexpression of fgf22 inhibited the generation of oligodendrocytes. Furthermore, the forebrain phenotypes of fgfr2b knockdown zebrafish were remarkably similar to those of fgf22 knockdown zebrafish. This establishes the Fgf22-Fgfr2b axis as a key ligand‒receptor partnership in neurogenesis and gliogenesis in the forebrain. Our results indicate that Fgf22 has a unique function in suppressing oligodendrocyte differentiation through Fgfr2b without affecting cell proliferation.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Zebrafish / Receptor, Fibroblast Growth Factor, Type 2 Type of study: Prognostic_studies Limits: Animals Language: En Journal: Biochem Biophys Res Commun Year: 2023 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Zebrafish / Receptor, Fibroblast Growth Factor, Type 2 Type of study: Prognostic_studies Limits: Animals Language: En Journal: Biochem Biophys Res Commun Year: 2023 Document type: Article