TY - JOUR T1 - DBZ Regulates Cortical Cell Positioning and Neurite Development by Sustaining the Anterograde Transport of Lis1 and DISC1 through Control of Ndel1 Dual-Phosphorylation JF - The Journal of Neuroscience JO - J. Neurosci. SP - 2942 LP - 2958 DO - 10.1523/JNEUROSCI.5029-13.2015 VL - 35 IS - 7 AU - Masayuki Okamoto AU - Tokuichi Iguchi AU - Tsuyoshi Hattori AU - Shinsuke Matsuzaki AU - Yoshihisa Koyama AU - Manabu Taniguchi AU - Munekazu Komada AU - Min-Jue Xie AU - Hideshi Yagi AU - Shoko Shimizu AU - Yoshiyuki Konishi AU - Minoru Omi AU - Tomohiko Yoshimi AU - Taro Tachibana AU - Shigeharu Fujieda AU - Taiichi Katayama AU - Akira Ito AU - Shinji Hirotsune AU - Masaya Tohyama AU - Makoto Sato Y1 - 2015/02/18 UR - http://www.jneurosci.org/content/35/7/2942.abstract N2 - Cell positioning and neuronal network formation are crucial for proper brain function. Disrupted-in-Schizophrenia 1 (DISC1) is anterogradely transported to the neurite tips, together with Lis1, and functions in neurite extension via suppression of GSK3β activity. Then, transported Lis1 is retrogradely transported and functions in cell migration. Here, we show that DISC1-binding zinc finger protein (DBZ), together with DISC1, regulates mouse cortical cell positioning and neurite development in vivo. DBZ hindered Ndel1 phosphorylation at threonine 219 and serine 251. DBZ depletion or expression of a double-phosphorylated mimetic form of Ndel1 impaired the transport of Lis1 and DISC1 to the neurite tips and hampered microtubule elongation. Moreover, application of DISC1 or a GSK3β inhibitor rescued the impairments caused by DBZ insufficiency or double-phosphorylated Ndel1 expression. We concluded that DBZ controls cell positioning and neurite development by interfering with Ndel1 from disproportionate phosphorylation, which is critical for appropriate anterograde transport of the DISC1-complex. ER -