一氧化氮的产生对于二氢神经酰胺诱导的烟草 BY-2 细胞死亡不是必需的。
Nitric oxide production is not required for dihydrosphingosine-induced cell death in tobacco BY-2 cells.
机构信息
Université de Toulouse, UPS, UMR 5546, Laboratoire de Recherche en Sciences Végétales, Castanet-Tolosan, France.
出版信息
Plant Signal Behav. 2011 May;6(5):736-9. doi: 10.4161/psb.6.5.15126. Epub 2011 May 1.
Abstract
Sphinganine or dihydrosphingosine (d18:0, DHS), one of the most abundant free sphingoid Long Chain Base (LCB) in plants, is known to induce a calcium dependent programmed cell death (PCD) in tobacco BY-2 cells. In addition, we have recently shown that DHS triggers a production of H2O2, via the activation of NADPH oxidase(s). However, this production of H2O2 is not correlated with the DHS-induced cell death but would rather be associated with basal cell defense mechanisms. In the present study, we extend our current knowledge of the DHS signaling pathway, by demonstrating that DHS also promotes a production of nitric oxide (NO) in tobacco BY-2 cells. As for H2O2, this NO production is not necessary for cell death induction.
摘要
神经醇或二氢神经鞘氨醇（d18:0，DHS）是植物中最丰富的游离神经鞘氨醇长链碱基（LCB）之一，已知它能诱导烟草 BY-2 细胞中依赖于钙的程序性细胞死亡（PCD）。此外，我们最近还表明，DHS 通过激活 NADPH 氧化酶（s）引发 H2O2 的产生。然而，这种 H2O2 的产生与 DHS 诱导的细胞死亡无关，而与基础细胞防御机制有关。在本研究中，我们通过证明 DHS 也能促进烟草 BY-2 细胞中一氧化氮（NO）的产生，扩展了我们对 DHS 信号通路的现有认识。与 H2O2 一样，这种 NO 的产生对于诱导细胞死亡不是必需的。
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