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

Arabidopsis thaliana MAP65-1 and MAP65-2 function redundantly with MAP65-3/PLEIADE in cytokinesis downstream of MPK4
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DOI:
10.4161/psb.6.5.15146
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发表时间:
2011-05
影响因子:
2.9
通讯作者:
M. Sasabe;Ken Kosetsu;M. Hidaka;A. Murase;Y. Machida
M. Sasabe;Ken Kosetsu;M. Hidaka;A. Murase;Y. Machida
中科院分区:
生物学4区
文献类型:
--
作者:
M. Sasabe;Ken Kosetsu;M. Hidaka;A. Murase;Y. Machida

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植物胞质分裂通过细胞板从细胞内部向细胞周边生长而发生。胞质分裂中的这些动态事件由称为成膜体的植物特异性微管(MT)阵列介导,所述成膜体由两个子核之间的成束反平行MT组成。NACK-PQR信号通路是一个由NACK 1驱动蛋白和丝裂原活化蛋白激酶(MAPK)级联反应组成的信号通路,通过调节成膜细胞膜蛋白来调控植物胞质分裂。MT相关蛋白MAP 65已被鉴定为参与细胞分裂的MT测定的结构组分之一,并且我们最近表明拟南芥AtMAP 65 -3/PLEIADE(PLE)是MPK 4的底物,MPK 4是拟南芥中NACK-PQR途径的组分。在这里,我们表明AtMAP 65 -1和AtMAP 65 -2也被MPK 4磷酸化。AtMAP 65 -1和AtMAP 65 -2在体外被MPK 4磷酸化。虽然拟南芥AtMAP 65 -1和AtMAP 65 -2基因的突变体表现出野生型表型,但AtMAP 65 -3和AtMAP 65 -1或AtMAP 65 -2的双突变引起比单一atmap 65 -3/ple突变更严重的生长和细胞动力学缺陷。这些结果表明AtMAP 65 -1和AtMAP 65 -2也在MPK 4下游的胞质分裂中起作用。
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.