Cell-cycle-dependent regulation of oxidative stress responses and Ca2+ permeable channels NtTPC1A/B in tobacco BY-2 cells
Cell-cycle-dependent regulation of oxidative stress responses and Ca2+ permeable channels NtTPC1A/B in tobacco BY-2 cells
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DOI：
10.1016/j.bbrc.2005.09.004
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发表时间：
2005-11-04
影响因子：
3.1
通讯作者：
Kuchitsu, K
中科院分区：
文献类型：
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作者：
Kadota, Y;Furuichi, T;Kuchitsu, K
植物总是暴露在氧化应激的威胁下，并通过激活多种防御反应来保护自己。然而，氧化应激诱导基因表达的分子机制在很大程度上尚不清楚。我们在这里研究了烟草 BY-2 细胞中氧化应激反应性推定电压依赖性 Ca2+ 通透通道 NtTPC1A 和 NtTPC1B 以及细胞周期在 H2O2 诱导的抗氧化酶、谷胱甘肽过氧化物酶 (GPX) 和抗坏血酸过氧化物酶 (APX) 表达中的作用。 H2O2 诱导的 [Ca2+](cyt) 升高以及 GPX 和 APX 的表达受到 NtTPC1A/B 和 Al 离子（NtTPC1s 的特异性阻断剂）共抑制的抑制，并通过 AtTPC1 的过表达而增强，表明 NtTPC1s 是 H2O2 激活的主要 Ca2+ 通透通道，并且通过 NtTPC1s 的 Ca2+ 流入参与了诱导H2O2 触发的基因表达。氧化应激诱导的信号转导机制高度依赖于细胞周期的各个阶段； H2O2 诱导的 [Ca2+](cyt) 升高以及 GPX 和 APX 的表达以及 NtTPC1s 转录物的水平彼此相关，并且在 G1 期达到最大。相反，已知与 NtTPC Is 无关的低渗休克诱导的 [Ca2+](cyt) 升高的细胞周期依赖性几乎相反，并且在 S 期达到最大。这些结果表明，氧化应激诱导的 [Ca2+](cyt) 升高和 NtTPC1 表达的细胞周期依赖性调节有助于 H2O2 诱导的过氧化物酶表达的细胞周期依赖性。各种 Ca2+ 介导的信号转导途径受细胞周期的差异调节。 (c) 2005 Elsevier Inc. 保留所有权利。
Plants are always exposed to the menace of oxidative stress and protect themselves by activating a variety of defense responses. However, molecular mechanisms for oxidative stress-induced gene expression are largely unknown. We here studied the roles of the oxidative stress-responsive putative voltage-dependent Ca2+ permeable channels, NtTPC1A and NtTPC1B, and cell cycle in H2O2-induced expression of antioxidant enzymes, glutathione peroxidase (GPX) and ascorbate peroxidase (APX) in tobacco BY-2 cells. H2O2-induced [Ca2+](cyt) rise and expression of GPX and APX were inhibited by the cosuppression of NtTPC1A/B as well as Al ion, a specific blocker for NtTPC1s, and enhanced by overexpression of AtTPC1, suggesting that NtTPC1s are the major Ca2+-permeable channels activated by H2O2 and that Ca2+ influx via NtTPC1s is involved in induction of H2O2-triggered gene expression. Oxidative stress-induced signal transduction mechanisms were highly dependent on the phases of the cell cycle; H2O2-induced [Ca2+](cyt) rise and expression of GPX and APX as well as the level of NtTPC1s transcripts correlated with each other and were maximal at G1 phase. In contrast, the cell cycledependence of hypoosmotic shock-induced [Ca2+](cyt) rise that is known to be independent of NtTPC Is was almost reverse and maximal at S phase. These results suggest that the cell cycle-dependent regulation of oxidative stress-induced [Ca2+](cyt) rise and expression of NtTPC1s contribute to the cell cycle dependence of H2O2-induced expression of peroxidases. Various Ca2+-mediated signal transduction pathways are differentially regulated by the cell cycle. (c) 2005 Elsevier Inc. All rights reserved.