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拟南芥 MAP65-1 和 MAP65-2 与 MAP65-3/PLEIADE 在 MPK4 下游的胞质分裂中具有冗余功能。

Arabidopsis thaliana MAP65-1 and MAP65-2 function redundantly with MAP65-3/PLEIADE in cytokinesis downstream of MPK4.

机构信息

Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya, Japan.

出版信息

Plant Signal Behav. 2011 May;6(5):743-7. doi: 10.4161/psb.6.5.15146. Epub 2011 May 1.

DOI:10.4161/psb.6.5.15146
PMID:21455028
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3172854/
Abstract

Plant cytokinesis occurs by the growth of cell plates from the interior to the periphery of the cell. These dynamic events in cytokinesis are mediated by a plant-specific microtubule (MT) array called the phragmoplast, which consists of bundled antiparallel MTs between the two daughter nuclei. The NACK-PQR pathway, a NACK1 kinesin-like protein and mitogen activated protein kinase (MAPK) cascade, is a key regulator of plant cytokinesis through the regulation of phragmoplast MTs. The MT-associated protein MAP65 has been identified as one of the structural components of MT assays involved in cell division, and we recently showed that Arabidopsis AtMAP65-3/PLEIADE (PLE) is a substrate of MPK4 that is a component of the NACK-PQR pathway in Arabidopsis. Here we show that AtMAP65-1 and AtMAP65-2 are also phosphorylated by MPK4. AtMAP65-1 and AtMAP65-2 that localize to the phragmoplast were phosphorylated by MPK4 in vitro. Although mutants of the Arabidopsis AtMAP65-1 and AtMAP65-2 genes exhibited a wild-type phenotype, double mutations of AtMAP65-3 and AtMAP65-1 or AtMAP65-2 caused more severe growth and cytokinetic defects than the single atmap65-3/ple mutation. These results suggest that AtMAP65-1 and AtMAP65-2 also function in cytokinesis downstream of MPK4.

摘要

植物细胞的胞质分裂是通过细胞板从细胞内部向细胞外周生长来实现的。这些胞质分裂过程中的动态事件是由一种称为成膜体的植物特异性微管(MT)阵列介导的,它由两个子核之间的束状平行 MT 组成。NACK-PQR 途径,一种 NACK1 类驱动蛋白和丝裂原活化蛋白激酶(MAPK)级联,是通过调节成膜体 MT 来调节植物胞质分裂的关键调节剂。MT 相关蛋白 MAP65 已被鉴定为参与细胞分裂的 MT 检测的结构成分之一,我们最近表明,拟南芥 AtMAP65-3/PLEIADE(PLE)是 NACK-PQR 途径中 MAPK4 的一个底物。在这里,我们表明 AtMAP65-1 和 AtMAP65-2 也被 MPK4 磷酸化。在体外,定位于成膜体的 AtMAP65-1 和 AtMAP65-2 被 MPK4 磷酸化。尽管拟南芥 AtMAP65-1 和 AtMAP65-2 基因的突变体表现出野生型表型,但 AtMAP65-3 和 AtMAP65-1 或 AtMAP65-2 的双突变导致比单个 atmap65-3/ple 突变更严重的生长和胞质分裂缺陷。这些结果表明 AtMAP65-1 和 AtMAP65-2 也在 MPK4 下游的胞质分裂中发挥作用。

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本文引用的文献

1
The MAP kinase MPK4 is required for cytokinesis in Arabidopsis thaliana.在拟南芥中,MAP 激酶 MPK4 对于胞质分裂是必需的。
Plant Cell. 2010 Nov;22(11):3778-90. doi: 10.1105/tpc.110.077164. Epub 2010 Nov 23.
2
HINKEL kinesin, ANP MAPKKKs and MKK6/ANQ MAPKK, which phosphorylates and activates MPK4 MAPK, constitute a pathway that is required for cytokinesis in Arabidopsis thaliana.HINKEL 驱动蛋白、ANP MAPKKKs 和 MKK6/ANQ MAPKK,它们磷酸化并激活 MPK4 MAPK,构成了拟南芥细胞分裂所必需的途径。
Plant Cell Physiol. 2010 Oct;51(10):1766-76. doi: 10.1093/pcp/pcq135. Epub 2010 Aug 27.
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Arabidopsis homologs of nucleus- and phragmoplast-localized kinase 2 and 3 and mitogen-activated protein kinase 4 are essential for microtubule organization.拟南芥核质体和纺锤体定位激酶 2 和 3 以及丝裂原活化蛋白激酶 4 的同源物对于微管组织是必需的。
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Arabidopsis microtubule-associated protein AtMAP65-2 acts as a microtubule stabilizer.拟南芥微管相关蛋白AtMAP65-2起到微管稳定剂的作用。
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MAP65-3 microtubule-associated protein is essential for nematode-induced giant cell ontogenesis in Arabidopsis.微管相关蛋白MAP65-3对于拟南芥中线虫诱导的巨细胞发生至关重要。
Plant Cell. 2008 Feb;20(2):423-37. doi: 10.1105/tpc.107.057422. Epub 2008 Feb 8.
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Control of the AtMAP65-1 interaction with microtubules through the cell cycle.通过细胞周期对AtMAP65-1与微管相互作用的调控。
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Phosphorylation of NtMAP65-1 by a MAP kinase down-regulates its activity of microtubule bundling and stimulates progression of cytokinesis of tobacco cells.丝裂原活化蛋白激酶对NtMAP65-1的磷酸化作用下调了其微管成束活性,并促进烟草细胞的胞质分裂进程。
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9
The rice mutant dwarf bamboo shoot 1: a leaky mutant of the NACK-type kinesin-like gene can initiate organ primordia but not organ development.水稻突变体矮化笋1:一种NACK型驱动蛋白样基因的渗漏突变体,可启动器官原基形成,但不能进行器官发育。
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10
Two microtubule-associated proteins of the Arabidopsis MAP65 family function differently on microtubules.拟南芥MAP65家族的两种微管相关蛋白在微管上的功能不同。
Plant Physiol. 2005 Jun;138(2):654-62. doi: 10.1104/pp.104.052456. Epub 2005 May 20.