Fig. 4: HDAC6 mediates acetyl-CoA-induced ciliogenesis in HSD17B4-deficient cells.
From: HSD17B4 deficiency causes dysregulation of primary cilia and is alleviated by acetyl-CoA
a Schematic diagram of HDAC inhibitors. HDAC inhibitors were categorized into classes I, IIa, IIb, and IV, with each HDAC inhibitor targeting a different class of HDAC. b–d HSD17B4-KO SY5Y/Cas9 cells were separately treated with the indicated HDAC inhibitors for 24 h. The cells were immunostained with an anti-ARL13B (green) antibody and Hoechst 33342 (blue) dye. Data are presented as the mean ± SEM (n = 3, independent biological replicates). P-value vs. treatment determined by one-way ANOVA followed by Tukey’s multiple comparisons test [Ciliated cells: Cont vs. Acetate p = 0.0128, PIC34051 p = 0.0202, Tubastatin A (Tuba A) p = 0.0002, TSA p < 0.0001, VPA p = 0.0001, SAHA p = 0.0002; Cilium length: Cont vs. Acetate, RGF966, TSA, SAHA p < 0.0001, Tuba A p = 0.0185, VPA p = 0.0145]. e–g The HDAC6-WT or -KO MEFs were transiently transfected with a Sc or siHSD17B4 (#1, #2) for 72 h. e, f The primary cilia were immunostained with an anti-ARL13B (green) antibody and the nuclei were counterstained with Hoechst 33342 (blue) dye. Data are presented as the mean ± SEM (n = 3, independent biological replicates). P-value vs. indicated groups determined by one-way ANOVA followed by Tukey’s multiple comparisons test [Ciliated cells: WT vs. HDAC6-KO; siHSD17B4 #1 p = 0.0016, siHSD17B4 #2 p = 0.0023; Cilium length: WT vs. HDAC6-KO; siHSD17B4 #1 p < 0.0001, siHSD17B4 #2 p < 0.0002]. Scale bar, 5 μm. g The upregulation of acetylated α-tubulin (Ac-α-tubulin) was assessed by western blotting analysis using the indicated antibody. Representative blot from three independent experiments is presented. Source data are provided as a Source Data file.
