Fig. 3

Mutant of the foxo1a gene leads to abnormal development of the telencephalon, oligodendrocytes, and myelin in zebrafish, as well as abnormal development of astrocytes and behavioral abnormalities.

A: Dorsal view of the brains of control and foxo1a^−/− larvae, the red coil indicates the position of the telencephalon.

B: Expression of olig2 fluorescent protein in the brains of control and foxo1a^−/− groups, with reduced fluorescence in the foxo1a^−/− group, scale bar = 100 μm

C: Representative transmission electron micrographs of myelin in control and foxo1a^−/− larvae, the yellow arrow indicates the location of the myelin, scale bar = 100 nm

D: In situ hybridization of olig2 and mbp in control and foxo1a^−/− groups.

E: qRT-PCR analysis of olig2, mbp, and plpa gene expression in oligodendrocytes of control and foxo1a^−/− zebrafish larvae, N = 6, t-test, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001

F: In situ hybridization of gfap in control and foxo1a^−/− groups.

G: Expression of gfap and s100b genes in astrocytes of control and foxo1a^−/− zebrafish larvae.,N = 6, t-test, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001

H: Comparison of glutamine synthetase activity in control and foxo1a^−/− zebrafish larvae, N = 6, t-test, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001

I: Schematic of the light-dark alternation behavior experiment, where the Viewpoint tool observes zebrafish for 90 min under normal daylight, followed by minute-by-minute light-dark alternations, and records the distance moved by control and foxo1a^−/− zebrafish larvae every 10 min.