A novel actin-microtubule cross-linking kinesin, NtKCH, functions in cell expansion and division

A novel actin-microtubule cross-linking kinesin, NtKCH, functions in cell expansion and division
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DOI:
10.1111/j.1469-8137.2011.03944.x
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发表时间:
2012-02-01
期刊:
影响因子:
9.4
通讯作者:
Nick, Peter
Nick, Peter
中科院分区:
生物学1区
文献类型:
--
作者:
Klotz, Jan;Nick, Peter

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具有钙调蛋白同源结构域(KCHs)的驱动蛋白最近被鉴定为驱动蛋白-14家族的植物特异性亚组,并且被怀疑充当微管肌动蛋白丝交联剂。然而,细胞功能仍然难以捉摸。为了解决KCH的功能,我们从烟草BY-2细胞中分离出一种新的KCH同源物NtKCH。同步后,NtKCH转录被证明是丰富的有丝分裂过程中,而在间期,表达低。使用荧光标记的细胞系和免疫标记技术,烟草KCH的本地化被发现不同的细胞周期。在间期,NtKCH主要与皮质微管,而一个亚馏分也共定位与核周肌动蛋白电缆。在分裂细胞中,NtKCH积累在前期带和成膜体。然而,它仍然没有从纺锤体微管,而是集中在两个聚集在两个细胞极附近。这项工作开发了一个详细的模型,在细胞分裂与细胞扩增的双重定位和功能的NtKCH。这个模型意味着两个动态的KCHs,不同的肌动蛋白相互作用。这允许在细胞周期依赖性捕获机制中通过KCH调节力的产生。
Kinesins with a calponin homology domain (KCHs) have been identified recently as a plant-specific subgroup of the kinesin-14 family and are suspected to act as microtubuleactin filament cross-linkers. The cellular function, however, has remained elusive. In order to address the function of KCHs, we isolated NtKCH, a novel KCH homologue from tobacco BY-2 cells. Following synchronization, NtKCH transcripts were shown to be abundant during mitosis, whereas, during interphase, expression was low. Using fluorescent-tagged cell lines and immunolabelling techniques, the localization of tobacco KCH was found to differ depending on the cell cycle. During interphase, NtKCH mainly associated with cortical microtubules, whereas a subfraction also co-localized with perinuclear actin cables. In dividing cells, NtKCH accumulated at the pre-prophase band and at the phragmoplast. However, it remained absent from spindle microtubules, but, instead, concentrated at two agglomerations in proximity to the two cell poles. This work develops a detailed model for the dual localization and function of NtKCH during cell division vs cell expansion. This model implies two dynamic states of KCHs that differ with regard to actin interaction. This allows the modulation of force generation by KCH in a cell cycle-dependent capture mechanism.