Sphingosine kinase AtSPHK1 functions in fumonisin B1-triggered cell death in Arabidopsis
Sphingosine kinase AtSPHK1 functions in fumonisin B1-triggered cell death in Arabidopsis
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鞘氨醇激酶 AtSPHK1 在伏马菌素 B1 触发的拟南芥细胞死亡中发挥作用
DOI：
10.1016/j.plaphy.2017.08.008
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发表时间：
2017-10-01
影响因子：
6.5
通讯作者：
Liang, Yun-Kuan
中科院分区：
文献类型：
--
作者：
Qin, Xiaoya;Zhang, Ruo-Xi;Liang, Yun-Kuan
真菌毒素伏马菌素B1 （Fumonisin B1， FBI）是一种强烈的诱诱剂，可以引发植物的超敏反应（hypersensitive responses， HR），同时增加长链碱基（LCB）和长链碱基磷酸盐（long chain base phosp磷酸盐，LCBP）含量，但FB1的调控机制以及LCB/LCBP信号盒在这一过程中的作用尚不完全清楚。在这里，我们报道了鞘氨酸激酶1 （SPHK1）通过调节拟南芥中水杨酸（SA）途径和活性氧（ROS）积累而成为fb1诱导HR的关键因子。SPHK1的过表达增加了fbi诱导的ROS和SA的积累。同时过表达SPHK1并抑制SPPASE或DPL1的双突变体比单独过表达SPHK1的植物对FBI、杀死和fb1诱导的SA激活的敏感性增强。SPHK1是SPPASE和DPL1两种主要负责植物鞘鞘醇-1-磷酸（Phyto-S1P）去除的酶。外源鞘氨醇-磷酸（S1P）可以以浓度依赖的双相方式调节SA应答标记基因PR1的转录。抑制SPHK1减少SA的产生，而促进茉莉酸（JA）的生物合成。我们的研究结果表明SPHK1通过SA和JA途径相互作用调节fb1触发的细胞死亡。(C) 2017年由Elsevier Masson SAS出版。
The fungal toxin Fumonisin B1 (FBI) is a strong inducer to trigger plant hypersensitive responses (HR) along with increased long chain bases (LCB) and long chain base phosphates (LCBP) contents, though the regulatory mechanism of FB1 action and how the LCB/LCBP signalling cassette functions during the process is still not fully understood. Here, we report sphingosine kinase 1 (SPHK1) as a key factor in FB1-induced HR by modulating the salicylic acid (SA) pathway and reactive oxygen species (ROS) accumulation in Arabidopsis thaliana. Overexpression of SPHK1 increases the FBI-induced accumulations of ROS and SA. The double mutant that simultaneously overexpresses SPHK1 and suppresses the SPPASE or DPL1, two enzymes are mainly responsible for Phyto-sphingosine-1-phosphate (Phyto-S1P) removal, showed enhanced susceptibility to FBI, killing and FB1-induced SA activation than the plants overexpress SPHK1 alone. Exogenous sphingosine-l-phosphate (S1P) can modulate the transcription of the SA responsive marker gene PR1 in a concentration-dependent biphasic manner. Suppression of SPHK1 decreases SA production whereas promotes jasmonic acid (JA) biosynthesis in response to FBI applications. Our findings indicate a role of SPHK1 in modulating FB1-triggered cell death via SA and JA pathway interactions. (C) 2017 Published by Elsevier Masson SAS.