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微管相关激酶样蛋白 RUNKEL 在体细胞和合胞体胞质分裂中发挥作用。

The microtubule-associated kinase-like protein RUNKEL functions in somatic and syncytial cytokinesis.

机构信息

ZMBP, Entwicklungsgenetik, Universität Tübingen, Auf der Morgenstelle 3, D-72076 Tübingen, Germany.

出版信息

Plant J. 2013 Jun;74(5):781-91. doi: 10.1111/tpj.12160. Epub 2013 Apr 10.

DOI:10.1111/tpj.12160
PMID:23451828
Abstract

The microtubule (MT)-associated putative kinase RUNKEL (RUK) is an important component of the phragmoplast machinery involved in cell plate formation in Arabidopsis somatic cytokinesis. Since loss-of-function ruk mutants display seedling lethality, it was previously not known whether RUK functions in mature sporophytes or during gametophyte development. In this study we utilized RUK proteins that lack the N-terminal kinase domain to further examine biological processes related to RUK function. Truncated RUK proteins when expressed in wild-type Arabidopsis plants cause cellularization defects not only in seedlings and adult tissues but also during male meiocyte development, resulting in abnormal pollen and reduced fertility. Ultrastructural analysis of male tetrads revealed irregular and incomplete or absent intersporal cell walls, caused by disorganized radial MT arrays. Moreover, in ruk mutants endosperm cellularization defects were also caused by disorganized radial MT arrays. Intriguingly, in seedlings expressing truncated RUK proteins, the kinesin HINKEL, which is required for the activation of a mitogen-activated protein kinase signaling pathway regulating phragmoplast expansion, was mislocalized. Together, these observations support a common role for RUK in both phragmoplast-based cytokinesis in somatic cells and syncytial cytokinesis in reproductive cells.

摘要

微管(MT)相关的假定激酶 RUNKEL(RUK)是参与拟南芥体细胞胞质分裂中细胞板形成的质膜体机器的重要组成部分。由于功能丧失的 ruk 突变体表现出幼苗致死性,因此之前尚不清楚 RUK 是否在成熟孢子体或配子体发育过程中发挥作用。在这项研究中,我们利用缺乏 N 端激酶结构域的 RUK 蛋白来进一步研究与 RUK 功能相关的生物学过程。在野生型拟南芥植物中表达的截断 RUK 蛋白不仅在幼苗和成年组织中,而且在雄性减数分裂细胞发育过程中引起细胞化缺陷,导致异常花粉和生育力降低。雄性四分体的超微结构分析显示,由于径向 MT 阵列的组织紊乱,导致孢子间细胞壁不规则、不完全或缺失。此外,在 ruk 突变体中,胚乳细胞化缺陷也是由径向 MT 阵列的组织紊乱引起的。有趣的是,在表达截断 RUK 蛋白的幼苗中,需要激活调节质膜体扩张的丝氨酸苏氨酸蛋白激酶信号通路的驱动蛋白 HINKEL 发生了定位错误。这些观察结果共同支持 RUK 在体细胞中基于质膜体的胞质分裂和生殖细胞中合胞体胞质分裂中的共同作用。

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