Arabidopsis Bax inhibitor-1 promotes sphingolipid synthesis during cold stress by interacting with ceramide-modifying enzymes
Arabidopsis Bax inhibitor-1 promotes sphingolipid synthesis during cold stress by interacting with ceramide-modifying enzymes
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DOI：
10.1007/s00425-014-2065-7
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发表时间：
2014-07-01
期刊：
影响因子：
4.3
通讯作者：
Kawai-Yamada, Maki
中科院分区：
文献类型：
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作者：
Nagano, Minoru;Ishikawa, Toshiki;Kawai-Yamada, Maki
Bax抑制因子-1(BI-1)是一种广泛保守的细胞死亡抑制因子，定位于内质网膜。我们以前的研究结果表明，拟南芥BI-1(Atbi-1)不仅与电子转移蛋白拟南芥细胞色素b(5)(Cb5)相互作用，而且还与含有Cb5LD结构域(Cb5LD)的蛋白-酿酒酵母脂肪酸2-羟基酶1相互作用，后者负责对鞘磷脂脂肪酸进行2-羟基化。我们现在已经发现Atbi-1与拟南芥鞘脂Delta 8长链碱基(LCB)脱饱和酶AtSLD1和AtSLD2结合，这两个蛋白都是含有Cb5LD的蛋白质。冷暴露后，Atbi-1和AtSLD1的表达均增加。然而，在Atbi-1突变体和sld1sld2双突变体之间，观察到了不同的表型对冷处理的反应。为了阐明差异背后的原因，我们分析了鞘脂，发现Atbi-1中的不饱和LCB与野生型相比没有变化，而sld1sld2中的LCB几乎都是饱和的，这表明Atbi-1可能不是LCBs去饱和所必需的。另一方面，野生型的鞘脂含量随着温度的升高而增加，而Atbi-1的总鞘脂含量没有变化。此外，神经酰胺修饰酶AtFAH1、鞘磷脂碱性羟基酶2(AtSBH2)、脂酰化脱氢酶2(AtADS2)和AtSLD1在低温胁迫下高表达，可能与Atbi-1的功能有关。这些发现表明，Atbi-1通过与AtSLD1、AtFAH1、AtSBH2和AtADS2相互作用，参与冷应激过程中鞘脂的合成。
Bax inhibitor-1 (BI-1) is a widely conserved cell death suppressor localized in the endoplasmic reticulum membrane. Our previous results revealed that Arabidopsis BI-1 (AtBI-1) interacts with not only Arabidopsis cytochrome b (5) (Cb5), an electron transfer protein, but also a Cb5-like domain (Cb5LD)-containing protein, Saccharomyces cerevisiae fatty acid 2-hydroxylase 1, which 2-hydroxylates sphingolipid fatty acids. We have now found that AtBI-1 binds Arabidopsis sphingolipid Delta 8 long-chain base (LCB) desaturases AtSLD1 and AtSLD2, which are Cb5LD-containing proteins. The expression of both AtBI-1 and AtSLD1 was increased by cold exposure. However, different phenotypes were observed in response to cold treatment between an atbi-1 mutant and a sld1sld2 double mutant. To elucidate the reasons behind the difference, we analyzed sphingolipids and found that unsaturated LCBs in atbi-1 were not altered compared to wild type, whereas almost all LCBs in sld1sld2 were saturated, suggesting that AtBI-1 may not be necessary for the desaturation of LCBs. On the other hand, the sphingolipid content in wild type increased in response to low temperature, whereas total sphingolipid levels in atbi-1 were unaltered. In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function. These findings suggest that AtBI-1 contributes to synthesis of sphingolipids during cold stress by interacting with AtSLD1, AtFAH1, AtSBH2 and AtADS2.