Fig. 5

5-HT6 regulated primary ciliary length through ARL13B. (a) CO-IP showed that 5-HT6 could bind with ARL13B in Hek293T cells. Bidirectional results showed that 5-HT6 and ARL13B interacted. (b) ARL13B restored the length of primary cilia. Cotransfection of ARL13B and 5-HT6 reduced cilia length, which was increased by overexpression of 5-HT6. (c) Ciliary length was shortened by expression of ARL13B. All groups were compared with the 5-HT6 group. Vector, **p < 0.01; ARL13B, **p < 0.01; 5-HT6 + ARL13B, **p < 0.01 (Kruskal–Wallis test, p < 0.001). (d) 5-HT6 had no effect on the total protein level of ARL13B in HEK293T cells. Kruskal–Wallis test, p = 0.85. GAPDH was the internal control. (e) D72A and F69L + T70I + D72A mutations of 5-HT6 influenced the quantity of cAMP (two-way ANOVA: concentration, F _6,12 = 5.45, p < 0.05; treatment, F _2,12 = 9.31, p < 0.01). Scale bars, 10 μm. All data presented as mean ± SEM (≥3 independent experiments). 5-HT6, serotonin 6 receptor, DAPI 4',6-diamidino-2-phenylindole, GFP green fluorescent protein