Cryptogein-Induced Cell Cycle Arrest at G2 Phase is Associated with Inhibition of Cyclin-Dependent Kinases, Suppression of Expression of Cell Cycle-Related Genes and Protein Degradation in Synchronized Tobacco BY-2 Cells
Cryptogein-Induced Cell Cycle Arrest at G2 Phase is Associated with Inhibition of Cyclin-Dependent Kinases, Suppression of Expression of Cell Cycle-Related Genes and Protein Degradation in Synchronized Tobacco BY-2 Cells
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DOI：
10.1093/pcp/pcr042
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发表时间：
2011-05-01
影响因子：
4.9
通讯作者：
Kuchitsu, Kazuyuki
中科院分区：
文献类型：
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作者：
Ohno, Ryoko;Kadota, Yasuhiro;Kuchitsu, Kazuyuki
病原菌或激发子诱导防御反应通常伴随着植物生长抑制，但其分子机制尚不清楚。在这篇报道中，我们描述了在同步培养的烟草亮黄-2 （BY-2）细胞中，隐基因素诱导的细胞周期阻滞在G(2)期所发生的分子事件。伴随着蛋白激发剂诱导的G(2)阻滞，我们观察到细胞周期蛋白依赖性激酶（CDKs）的组蛋白H1激酶活性受到抑制，这与CDKB1 mRNA和蛋白水平的降低相关。相比之下，即使在M期，CDKA的数量也几乎不受cryptoin的影响。cryptoin不仅能快速抑制阳性细胞周期蛋白（如A型和b型细胞周期蛋白和NtCAK）的表达，还能抑制阴性细胞周期调节因子（如WEE1）的表达，这表明cryptoin通过不同于已知检查点调节的机制影响多个靶点，使CDKA失活，从而诱导G(2)阻滞。此外，我们发现CDKB1和细胞周期蛋白也被隐基因快速降解，蛋白酶体依赖的蛋白质降解在控制隐基因诱导的超敏性细胞死亡中起着至关重要的作用。
Induction of defense responses by pathogens or elicitors is often accompanied by growth inhibition in planta, but its molecular mechanisms are poorly understood. In this report, we characterized the molecular events that occur during cryptogein-induced cell cycle arrest at G(2) phase in synchronously cultured tobacco Bright Yellow-2 (BY-2) cells. Concomitant with the proteinaceous elicitor-induced G(2) arrest, we observed inhibition of the histone H1 kinase activity of cyclin-dependent kinases (CDKs), which correlated with a decrease in mRNA and protein levels of CDKB1. In contrast, the amount of CDKA was almost unaffected by cryptogein even at M phase. Cryptogein rapidly inhibited the expression not only of positive, e.g. A- and B-type cyclins and NtCAK, but also of negative cell cycle regulators such as WEE1, suggesting that cryptogein affects multiple targets to inactivate CDKA to induce G(2) arrest by mechanisms distinct from known checkpoint regulation. Moreover, we show that CDKB1 and cyclin proteins are also rapidly degraded by cryptogein and that the proteasome-dependent protein degradation has a crucial role in the control of cryptogein-induced hypersensitive cell death.