Ethylene Modulates Sphingolipid Synthesis in Arabidopsis.
Ethylene Modulates Sphingolipid Synthesis in Arabidopsis.
复制标题
乙烯调节拟南芥中的鞘脂合成。
DOI：
10.3389/fpls.2015.01122
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发表时间：
2015
影响因子：
5.6
通讯作者：
Yao N
中科院分区：
文献类型：
--
作者：
Wu JX;Wu JL;Yin J;Zheng P;Yao N
鞘脂在膜和信号传导中具有重要的结构和生物活性功能。然而，植物如何调节鞘脂的生物合成在应对压力仍然不清楚。在这里，我们揭示了植物激素乙烯可以调节鞘脂的合成。真菌毒素伏马菌素B1（FB 1）抑制神经酰胺脱氢酶的活性，扰乱鞘脂体内平衡，从而诱导细胞死亡。我们使用FB 1来测试乙烯信号在拟南芥鞘脂合成中的作用。etr 1 -1和ein 2突变体，破坏乙烯信号，表现出对FB 1的超敏反应;相反，eto 1 -1和ctr 1 -1突变体，增强乙烯信号，表现出增加的耐受性FB 1。基因表达分析表明，在FB 1处理，转录参与从头鞘脂生物合成的基因下调ctr 1 -1突变体，但上调ein 2突变体。引人注目的是，在正常条件下，与野生型相比，ctr 1 -1突变体含有较少的神经酰胺和羟基神经酰胺。FB 1处理后，ctr 1 -1和ein 2突变体表现出显着改善鞘脂含量，除了ctr 1 -1突变体表现出羟基神经酰胺水平的变化不大。用乙烯前体1-氨基环丙烷羧酸处理野生型幼苗下调了参与鞘脂从头生物合成途径的基因，从而降低了鞘脂含量并部分挽救了FB 1诱导的细胞死亡。综合这些结果，我们认为乙烯通过调节鞘脂从头生物合成相关基因的表达来调节鞘脂。
Sphingolipids have essential structural and bioactive functions in membranes and in signaling. However, how plants regulate sphingolipid biosynthesis in the response to stress remains unclear. Here, we reveal that the plant hormone ethylene can modulate sphingolipid synthesis. The fungal toxin Fumonisin B1 (FB1) inhibits the activity of ceramide synthases, perturbing sphingolipid homeostasis, and thus inducing cell death. We used FB1 to test the role of ethylene signaling in sphingolipid synthesis in Arabidopsis thaliana. The etr1-1 and ein2 mutants, which have disrupted ethylene signaling, exhibited hypersensitivity to FB1; by contrast, the eto1-1 and ctr1-1 mutants, which have enhanced ethylene signaling, exhibited increased tolerance to FB1. Gene expression analysis showed that during FB1 treatment, transcripts of genes involved in de novo sphingolipid biosynthesis were down-regulated in ctr1-1 mutants but up-regulated in ein2 mutants. Strikingly, under normal conditions, ctr1-1 mutants contained less ceramides and hydroxyceramides, compared with wild type. After FB1 treatment, ctr1-1 and ein2 mutants showed a significant improvement in sphingolipid contents, except the ctr1-1 mutants showed little change in hydroxyceramide levels. Treatment of wild-type seedlings with the ethylene precursor 1-aminocyclopropane carboxylic acid down-regulated genes involved in the sphingolipid de novo biosynthesis pathway, thus reducing sphingolipid contents and partially rescuing FB1-induced cell death. Taking these results together, we propose that ethylene modulates sphingolipids by regulating the expression of genes related to the de novo biosynthesis of sphingolipids.