The elongation of primary cilia via the acetylation of alpha-tubulin by the treatment with lithium chloride in human fibroblast KD cells

Primary cilium, an organelle found on nearly every cell in the human body, typically serves as the mechanical sensor of the cell. Lithium ion is known to promote the elongation of primary cilia in a variety of cell types, but it is unknown whether lithium is involved in the acetylation of alpha-tubulin which is essential for the assembly of primary cilia. In order to reveal the relationship between the elongation of primary cilia with lithium and the acetylation of alpha-tubulin, we first observed the formation and structure of primary cilia in KD cells, a cell line deriving fibroblasts in human labium. Subsequently, by immunohistochemical and western blot analysis we elucidated that the length of primary cilia and acetylation of alpha-tubulin are regulated by lithium chloride (LiCl) in the medium in a time- and concentration-dependent manner. We next performed the RT-PCR, RNAi-based experiments and biochemical study using an inhibitor of glycogen synthase kinase-3 beta GSK-3 beta). We found that LiCl mobilizes the alpha-tubulin N-acetyltransferase 1 (alpha TAT1) in the signaling pathway mediating GSK-3 beta and adenylate cyclase III. In conclusion, our results suggested that LiCl treatments activate alpha TAT1 by the inhibition of GSK-3 beta and promote the alpha-tubulin acetylation, and then elongate the primary cilia.