Sphingolipid long chain base phosphates can regulate apoptotic-like programmed cell death in plants
Sphingolipid long chain base phosphates can regulate apoptotic-like programmed cell death in plants
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DOI：
10.1016/j.bbrc.2011.06.028
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发表时间：
2011-07-08
影响因子：
3.1
通讯作者：
Leaver, Christopher J.
中科院分区：
文献类型：
--
作者：
Alden, Keith P.;Dhondt-Cordelier, Sandrine;Leaver, Christopher J.
鞘脂是真核细胞中普遍存在的组分，鞘脂代谢物，如长链碱性磷酸盐（LCB-P）、鞘氨醇1磷酸盐（SiP）和神经酰胺（Cer）是动物细胞凋亡的重要调节剂。本研究使用市售的S1 P作为工具，评估LCB-Ps在调节植物细胞中的类拟南芥程序性细胞死亡（AL-PCD）中的作用。拟南芥细胞培养物暴露于一系列不同的细胞死亡诱导治疗（包括Cer）的存在下的Si P.率的AL-PCD和细胞存活率记录使用重要的染色和AL-PCD的形态标记。使用鞘氨醇激酶抑制剂在悬浮培养细胞中改变内部LCB-P水平，并评估热应激反应中死亡率的变化。S1 P减少了AL-PCD并促进了受到一系列应激的细胞的存活。用鞘氨醇激酶抑制剂处理降低了细胞培养物中诱导最大AL-PCD的温度。这些数据支持存在一个鞘脂变阻器参与控制细胞的命运在拟南芥细胞和鞘脂调节细胞死亡可能是动物细胞凋亡和植物AL-PCD的共同特征。(C)2011 Elsevier Inc. All rights reserved.
Sphingolipids are ubiquitous components of eukaryotic cells and sphingolipid metabolites, such as the long chain base phosphate (LCB-P), sphingosine 1 phosphate (Si P) and ceramide (Cer) are important regulators of apoptosis in animal cells. This study evaluated the role of LCB-Ps in regulating apoptotic-like programmed cell death (AL-PCD) in plant cells using commercially available S1P as a tool. Arabidopsis cell cultures were exposed to a diverse array of cell death-inducing treatments (including Cer) in the presence of Si P. Rates of AL-PCD and cell survival were recorded using vital stains and morphological markers of AL-PCD. Internal LCB-P levels were altered in suspension cultured cells using inhibitors of sphingosine kinase and changes in rates of death in response to heat stress were evaluated. S1P reduced AL-PCD and promoted cell survival in cells subjected to a range of stresses. Treatments with inhibitors of sphingosine kinase lowered the temperature which induced maximal AL-PCD in cell cultures. The data supports the existence of a sphingolipid rheostat involved in controlling cell fate in Arabidopsis cells and that sphingolipid regulation of cell death may be a shared feature of both animal apoptosis and plant AL-PCD. (C) 2011 Elsevier Inc. All rights reserved.