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首页> 外文期刊>Cell Research >Involvement of sphingoid bases in mediating reactive oxygen intermediate production and programmed cell death in Arabidopsis
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Involvement of sphingoid bases in mediating reactive oxygen intermediate production and programmed cell death in Arabidopsis

机译：鞘氨醇碱基参与介导拟南芥中活性氧中间产物的产生和程序性细胞死亡

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摘要

Sphingolipids have been suggested to act as second messengers for an array of cellular signaling activities in plant cells, including stress responses and programmed cell death (PCD). However, the mechanisms underpinning these processes are not well understood. Here, we report that an Arabidopsis mutant, fumonisin B1 resistant11-1 (fbr 11-1), which fails to generate reactive oxygen intermediates (ROIs), is incapable of initiating PCD when the mutant is challenged by fumonisin B_1 (FB_1), a specific inhibitor of ceramide synthase. Molecular analysis indicated that FBR11 encodes a long-chain basel (LCB1) subunit of serine palmitoyltransferase (SPT), which catalyzes the first rate-limiting step of de novo sphingolipid synthesis. Mass spectrometric analysis of the sphingolipid concentrations revealed that whereas the fbr 11-1 mutation did not affect basal levels of sphingoid bases, the mutant showed attenuated formation of sphingoid bases in response to FB_1. By a direct feeding experiment, we show that the free sphingoid bases dihydrosphingosine, phytosphingosine and sphingosine efficiently induce ROI generation followed by cell death. Conversely, ROI generation and cell death induced by dihydrosphingosine were specifically blocked by its phosphorylated form dihydrosphingosine-1-phosphate in a dose-dependent manner, suggesting that the maintenance of homeostasis between a free sphingoid base and its phosphorylated derivative is critical to determining the cell fate. Because alterations of the sphingolipid level occur prior to the ROI production, we propose that the free sphingoid bases are involved in the control of PCD in Arabidopsis, presumably through the regulation of the ROI level upon receiving different developmental or environmental cues.
机译：已经提出鞘脂充当植物细胞中一系列细胞信号传导活性的第二信使，包括应激反应和程序性细胞死亡（PCD）。但是，支撑这些过程的机制尚不十分清楚。在这里，我们报道了当拟南芥突变体受到伏马菌素B_1（FB_1）的攻击时，不能产生活性氧中间体（ROIs）的拟南芥突变体fumonisin B1抗性11-1（fbr 11-1）无法启动PCD。神经酰胺合酶的特异性抑制剂。分子分析表明，FBR11编码丝氨酸棕榈酰转移酶（SPT）的长链碱基（LCB1）亚基，它催化从头鞘脂合成的第一步限速步骤。鞘脂浓度的质谱分析表明，尽管fbr 11-1突变不影响鞘氨醇碱基的基础水平，但该突变体显示响应FB_1减少了鞘氨醇碱基的形成。通过直接进食实验，我们显示了游离的鞘氨醇碱基二氢鞘氨醇，植物鞘氨醇和鞘氨醇有效诱导了ROI的产生，随后细胞死亡。相反，由二氢鞘氨醇诱导的ROI生成和细胞死亡被其磷酸化形式二氢鞘氨醇-1-磷酸以剂量依赖性方式特异性阻断，这表明维持游离鞘氨醇碱基与其磷酸化衍生物之间的体内平衡对于确定细胞至关重要。命运。因为鞘脂水平的变化发生在ROI产生之前，所以我们建议拟南芥中游离的鞘氨醇碱基参与PCD的控制，大概是通过在接受不同的发育或环境线索时调节ROI水平。

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