Nature Publishing Group Acta Medica Okayama 20452322 7 2017 Directional cell expansion requires NIMA-related kinase 6 (NEK6)-mediated cortical microtubule destabilization; 7826 EN Shogo Takatani Department of Biological Science, Graduate School of Natural Science and Technology, Okayama University Shinichiro Ozawa Department of Biological Science, Graduate School of Natural Science and Technology, Okayama University Noriyoshi Yagi Graduate School of Biological Science, Nara Institute of Science and Technology Takashi Hotta Graduate School of Biological Science, Nara Institute of Science and Technology Takashi Hashimoto Graduate School of Biological Science, Nara Institute of Science and Technology Yuichiro Takahashi Graduate School of Natural Science and Technology/Faculty of Science, Okayama University Taku Takahashi Department of Biological Science, Graduate School of Natural Science and Technology, Okayama University Hiroyasu Motose Department of Biological Science, Graduate School of Natural Science and Technology, Okayama University 　Plant cortical microtubules align perpendicular to the growth axis to determine the direction of cell growth. However, it remains unclear how plant cells form well-organized cortical microtubule arrays in the absence of a centrosome. In this study, we investigated the functions of Arabidopsis NIMA-related kinase 6 (NEK6), which regulates microtubule organization during anisotropic cell expansion. Quantitative analysis of hypocotyl cell growth in the nek6-1 mutant demonstrated that NEK6 suppresses ectopic outgrowth and promotes cell elongation in different regions of the hypocotyl. Loss of NEK6 function led to excessive microtubule waving and distortion, implying that NEK6 suppresses the aberrant cortical microtubules. Live cell imaging showed that NEK6 localizes to the microtubule lattice and to the shrinking plus and minus ends of microtubules. In agreement with this observation, the induced overexpression of NEK6 reduced and disorganized cortical microtubules and suppressed cell elongation. Furthermore, we identified five phosphorylation sites in β-tubulin that serve as substrates for NEK6 in vitro. Alanine substitution of the phosphorylation site Thr166 promoted incorporation of mutant β-tubulin into microtubules. Taken together, these results suggest that NEK6 promotes directional cell growth through phosphorylation of β-tubulin and the resulting destabilization of cortical microtubules. No potential conflict of interest relevant to this article was reported.