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拟南芥细胞周期蛋白依赖性激酶抑制剂 ICK3/KRP5 对主根生长起限速作用,并通过细胞伸长和核内有丝分裂促进生长。

The Arabidopsis CDK inhibitor ICK3/KRP5 is rate limiting for primary root growth and promotes growth through cell elongation and endoreduplication.

机构信息

School of Biosciences, Cardiff University, Museum Avenue, Cardiff, UK.

出版信息

J Exp Bot. 2013 Feb;64(4):1135-44. doi: 10.1093/jxb/ert009.

Abstract

The coordination of plant cell division and expansion controls plant morphogenesis, development, and growth. Cyclin-dependent kinases (CDKs) are not only key regulators of cell division but also play an important role in cell differentiation. In plants, CDK activity is modulated by the binding of INHIBITOR OF CDK/KIP-RELATED PROTEIN (ICK/KRP). Previously, ICK2/KRP2 has been shown to mediate auxin responses in lateral root initiation. Here are analysed the roles of all ICK/KRP genes in root growth. Analysis of ick/krp null-mutants revealed that only ick3/krp5 was affected in primary root growth. ICK3/KRP5 is strongly expressed in the root apical meristem (RAM), with lower expression in the expansion zone. ick3/krp5 roots grow more slowly than wildtype controls, and this results not from reduction of division in the proliferative region of the RAM but rather reduced expansion as cells exit the meristem. This leads to shorter final cell lengths in different tissues of the ick3/krp5 mutant root, particularly the epidermal non-hair cells, and this reduction in cell size correlates with reduced endoreduplication. Loss of ICK3/KRP5 also leads to delayed germination and in the mature embryo ICK3/KRP5 is specifically expressed in the transition zone between root and hypocotyl. Cells in the transition zone were smaller in the ick3/krp5 mutant, despite the absence of endoreduplication in the embryo suggesting a direct effect of ICK3/KRP5 on cell growth. It is concluded that ICK3/KRP5 is a positive regulator of both cell growth and endoreduplication.

摘要

植物细胞分裂和扩张的协调控制着植物形态发生、发育和生长。细胞周期蛋白依赖性激酶(CDK)不仅是细胞分裂的关键调节因子,而且在细胞分化中也起着重要作用。在植物中,CDK 的活性通过 INHIBITOR OF CDK/KIP-RELATED PROTEIN(ICK/KRP)的结合来调节。先前,ICK2/KRP2 已被证明介导了侧根起始中的生长素反应。这里分析了所有 ICK/KRP 基因在根生长中的作用。对 ick/krp 缺失突变体的分析表明,只有 ick3/krp5 受到主根生长的影响。ICK3/KRP5 在根顶端分生组织(RAM)中强烈表达,在扩展区表达较低。ick3/krp5 根比野生型对照生长得更慢,这不是由于 RAM 增殖区的分裂减少,而是由于细胞离开分生组织时的扩展减少。这导致 ick3/krp5 突变根的不同组织中的最终细胞长度变短,特别是表皮非毛细胞,并且这种细胞大小的减少与内复制减少相关。ICK3/KRP5 的缺失也导致萌发延迟,并且在成熟胚胎中,ICK3/KRP5 特异性表达在根和下胚轴之间的过渡区。尽管胚胎中没有内复制,但过渡区的细胞在 ick3/krp5 突变体中较小,这表明 ICK3/KRP5 对细胞生长有直接影响。综上所述,ICK3/KRP5 是细胞生长和内复制的正调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4410/3580825/8bf65e7b2037/exbotj_ert009_f0001.jpg

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