Hosoba Kosuke, Komatsu Satoshi, Ikebe Mitsuo, Kotani Manato, Wenqin Xiao, Tachibana Taro, Hosoya Hiroshi, Hamao Kozue
Department of Biological Science, Graduate School of Science, Hiroshima University, Higashi-Hiroshima 739-8526, Japan.
Department of Cellular and Molecular Biology, University of Texas Health Northeast, Tyler, TX 75708, USA.
Biochem Biophys Res Commun. 2015 Apr 17;459(4):686-91. doi: 10.1016/j.bbrc.2015.03.005. Epub 2015 Mar 11.
Zipper-interacting protein kinase (ZIPK) is known to regulate several functions such as apoptosis, smooth muscle contraction, and cell migration. While exogenously expressed GFP-ZIPK localizes to the cleavage furrow, role of ZIPK in cytokinesis is obscure. Here, we show that ZIPK is a major MRLC kinase during mitosis. Moreover, ZIPK siRNA-mediated knockdown causes delay of cytokinesis. The delay in cytokinesis of ZIPK-knockdown cells was rescued by the exogenous diphosphorylation-mimicking MRLC mutant. Taken together, these findings suggest that ZIPK plays a role in the progression and completion of cytokinesis through MRLC phosphorylation.
已知拉链相互作用蛋白激酶(ZIPK)可调节多种功能,如细胞凋亡、平滑肌收缩和细胞迁移。虽然外源表达的绿色荧光蛋白-ZIPK定位于分裂沟,但ZIPK在胞质分裂中的作用尚不清楚。在这里,我们表明ZIPK是有丝分裂期间的主要肌球蛋白轻链激酶(MRLC激酶)。此外,ZIPK siRNA介导的敲低会导致胞质分裂延迟。外源表达的模拟双磷酸化的MRLC突变体挽救了ZIPK敲低细胞的胞质分裂延迟。综上所述,这些发现表明ZIPK通过MRLC磷酸化在胞质分裂的进程和完成中发挥作用。