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III 类代偿,以 KRP2 过表达为代表,依赖于增殖细胞中的 V-ATPase 活性。

Class III compensation, represented by KRP2 overexpression, depends on V-ATPase activity in proliferative cells.

机构信息

Department of Biology; Tokyo Gakugei University; Koganei-shi, Japan.

Laboratory of Cell Dynamics; Graduate School of Bioagricultural Sciences; Nagoya University; Nagoya, Japan.

出版信息

Plant Signal Behav. 2013 Nov;8(11):e27204. doi: 10.4161/psb.27204. Epub 2013 Dec 4.

Abstract

Compensation refers to an increase in cell size when the cell number is significantly decreased due to the mutation or gain of function of a gene that negatively affects the cell cycle. Given the importance of coordinated growth during organogenesis in both animal and plant systems, compensation is important to understand the mechanism of size regulation. In leaves, cell division precedes cell differentiation (which involves cell expansion); therefore, a decrease in cell number triggers enhanced cell expansion (compensated cell expansion; hereafter, CCE). Functional analyses of genes for which a loss or gain of function triggers compensation have increased our understanding of the molecular mechanisms underlying the decrease in cell number. Nevertheless, the mechanisms that induce enhanced cell expansion (the link between cell cycling and expansion), as well as the cellular machinery mediating CCE, have not been characterized. We recently characterized an important pathway involved in cell enlargement in KRP2-overexpressing plants. Here, we discuss the potential axial role of plant KRPs in triggering enlargement in cells with meristematic features.

摘要

补偿是指当细胞数量因基因的突变或功能获得而显著减少,从而对细胞周期产生负面影响时,细胞大小的增加。鉴于在动物和植物系统中器官发生过程中协调生长的重要性,了解大小调节的机制,补偿是很重要的。在叶片中,细胞分裂先于细胞分化(涉及细胞扩张);因此,细胞数量的减少会引发细胞的强烈扩张(补偿性细胞扩张;以下简称 CCE)。对那些功能丧失或获得会引发补偿的基因进行功能分析,增加了我们对细胞数量减少的分子机制的理解。然而,诱导细胞强烈扩张的机制(细胞循环和扩张之间的联系),以及介导 CCE 的细胞机制,尚未被描述。我们最近对 KRP2 过表达植物中参与细胞扩大的重要途径进行了特征描述。在这里,我们讨论了植物 KRPs 在触发具有分生组织特征的细胞增大中的潜在轴向作用。

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