Department of Gene Function and Phenomics, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
Nikon Imaging Center, Research Institute for Electronic Science, Hokkaido University, Sapporo, Hokkaido 001-0020, Japan.
Curr Biol. 2019 Dec 2;29(23):4060-4070.e3. doi: 10.1016/j.cub.2019.09.049. Epub 2019 Nov 14.
Cytokinesis is fundamental for cell proliferation [1, 2]. In plants, a bipolar short-microtubule array forms the phragmoplast, which mediates vesicle transport to the midzone and guides the formation of cell walls that separate the mother cell into two daughter cells [2]. The phragmoplast centrifugally expands toward the cell cortex to guide cell-plate formation at the cortical division site [3, 4]. Several proteins in the phragmoplast midzone facilitate the anti-parallel bundling of microtubules and vesicle accumulation [5]. However, the mechanisms by which short microtubules are maintained during phragmoplast development, in particular, the behavior of microtubules at the distal zone of phragmoplasts, are poorly understood. Here, we show that a plant-specific protein, CORTICAL MICROTUBULE DISORDERING 4 (CORD4), tethers the conserved microtubule-severing protein katanin to facilitate formation of the short-microtubule array in phragmoplasts. CORD4 was specifically expressed during mitosis and localized to preprophase bands and phragmoplast microtubules. Custom-made two-photon spinning disk confocal microscopy revealed that CORD4 rapidly localized to microtubules in the distal phragmoplast zone during phragmoplast assembly at late anaphase and persisted throughout phragmoplast expansion. Loss of CORD4 caused abnormally long and oblique phragmoplast microtubules and slow expansion of phragmoplasts. The p60 katanin subunit, KTN1, localized to the distal phragmoplast zone in a CORD4-dependent manner. These results suggest that CORD4 tethers KTN1 at phragmoplasts to modulate microtubule length, thereby accelerating phragmoplast growth. This reveals the presence of a distinct machinery to accelerate cytokinesis by regulating the action of katanin.
有丝分裂对于细胞增殖至关重要[1,2]。在植物中，一个双极短微管阵列形成成膜体，它介导囊泡运输到中区，并指导细胞壁的形成，将母细胞分隔成两个子细胞[2]。成膜体向细胞皮层离心扩展，指导在皮层分裂位点形成细胞板[3,4]。成膜体中部的几种蛋白质促进微管的反平行束集和囊泡积累[5]。然而，在成膜体发育过程中短微管如何被维持，特别是成膜体远区微管的行为，知之甚少。在这里，我们表明，一种植物特异性蛋白 CORTICAL MICROTUBULE DISORDERING 4 (CORD4) 将保守的微管切割蛋白katanin 固定在成膜体中，以促进短微管阵列的形成。CORD4 在有丝分裂期间特异性表达，定位在前期带和成膜体微管上。定制的双光子旋转盘共聚焦显微镜显示，在后期有丝分裂末期成膜体组装期间，CORD4 快速定位到成膜体远区的微管上，并在成膜体扩展过程中持续存在。CORD4 的缺失导致成膜体微管异常长且倾斜，成膜体扩展缓慢。p60 katanin 亚基 KTN1 以 CORD4 依赖的方式定位到成膜体的远区。这些结果表明，CORD4 将 KTN1 固定在成膜体上，调节微管长度，从而加速成膜体生长。这揭示了存在一种独特的机制，通过调节katanin 的作用来加速细胞分裂。
