discordia mutations specifically misorient asymmetric cell divisions during development of the maize leaf epidermis.

discordia mutations specifically misorient asymmetric cell divisions during development of the maize leaf epidermis.
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发表时间:
1999-10
期刊:
影响因子:
4.6
通讯作者:
Kim Gallagher;Laurie G. Smith
Kim Gallagher;Laurie G. Smith
中科院分区:
生物学2区
文献类型:
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作者:
Kim Gallagher;Laurie G. Smith

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在植物细胞中,胞质分裂依赖于称为成膜体的细胞骨架结构,其指导有丝分裂后子核之间新细胞壁的形成。细胞分裂的方向取决于在胞质分裂期间成膜体对皮质部位的引导,该皮质部位在整个前期由另一种称为前前期带的细胞骨架结构标记。不对称分裂的细胞在有丝分裂前变得极化并形成不对称的preprophase带;成膜体随后被引导到这些不对称的皮质部位以形成不同形状和/或大小的子细胞。在这里,我们描述了两个新的隐性突变,discordia 1(dcd 1)和discordia 2(dcd 2),这破坏了不对称细胞分裂过程中胞质分裂的空间调控。这两种突变破坏了四类不对称细胞分裂过程中的玉米叶表皮的发展,而不影响对称分裂,通过大多数表皮细胞出现。dcd突变对不对称细胞分裂的影响可以通过细胞松弛素D处理来模拟,并且受dcd 1影响的分裂对细胞松弛素D的影响非常敏感。肌动蛋白和微管组织在这些突变体的分析表明,无论是对细胞极性的突变,或对preprophase带和纺锤体的形成和定位没有影响。在突变细胞中,不对称分裂细胞中的成膜体在结构上是正常的,并且在正确的位置开始,但通常不能移动到以前由preprophase带占据的位置。我们认为dcd突变破坏了不对称分裂细胞胞质分裂过程中指导成膜体的肌动蛋白依赖过程。
In plant cells, cytokinesis depends on a cytoskeletal structure called a phragmoplast, which directs the formation of a new cell wall between daughter nuclei after mitosis. The orientation of cell division depends on guidance of the phragmoplast during cytokinesis to a cortical site marked throughout prophase by another cytoskeletal structure called a preprophase band. Asymmetrically dividing cells become polarized and form asymmetric preprophase bands prior to mitosis; phragmoplasts are subsequently guided to these asymmetric cortical sites to form daughter cells of different shapes and/or sizes. Here we describe two new recessive mutations, discordia1 (dcd1) and discordia2 (dcd2), which disrupt the spatial regulation of cytokinesis during asymmetric cell divisions. Both mutations disrupt four classes of asymmetric cell divisions during the development of the maize leaf epidermis, without affecting the symmetric divisions through which most epidermal cells arise. The effects of dcd mutations on asymmetric cell division can be mimicked by cytochalasin D treatment, and divisions affected by dcd1 are hypersensitive to the effects of cytochalasin D. Analysis of actin and microtubule organization in these mutants showed no effect of either mutation on cell polarity, or on formation and localization of preprophase bands and spindles. In mutant cells, phragmoplasts in asymmetrically dividing cells are structurally normal and are initiated in the correct location, but often fail to move to the position formerly occupied by the preprophase band. We propose that dcd mutations disrupt an actin-dependent process necessary for the guidance of phragmoplasts during cytokinesis in asymmetrically dividing cells.