儿茶素诱导的拟南芥根细胞膜脂变化(英文)

Profiling of Membrane Lipids of Arabidopsis Roots during Catechin Treatment

儿茶素是一种可以短时间内杀死植物细胞的植物毒素,由于具有强的植物毒性,儿茶素是开发除草剂的理想化合物,它可以诱导植物根系统的死亡。为了研究植物根细胞膜脂对化学胁迫的响应规律,我们运用高通量的脂类组学方法检测了拟南芥根中膜脂分子的组成,比较了儿茶素处理下拟南芥野生型(WS)及磷脂酶Dδ缺失突变体(PLDδ-KO)根中膜脂分子的组成情况、膜脂含量、双键指数及碳链长度值。结果发现,儿茶素处理拟南芥根90min后,二半乳糖基二酰甘油(DGDG)、单半乳糖基二酰甘油(MG-DG)、磷脂酰甘油(PG)、磷脂酰胆碱(PC)及磷脂酰肌醇(PI)的总含量在WS与PLDδ-KO植株根中都显著下降,磷脂酰乙醇胺(PE)和磷脂酰丝氨酸(PS)在WS中下降,在PLDδ-KO中上升。儿茶素处理导致PLDδ-KO植株的PC/PE比值显著下降,WS植株PS碳链长度显著增加。上述结果说明儿茶素处理后,磷脂酶Dδ缺失突变体膜不稳定性增加,PLDδ-KO植株对儿茶素胁迫更加敏感。

Catechin is a kind of phytotoxin and can kill plant cells in an hour. It can be developed as herbicide to kill weeds due to its strong phytotoxic activity. The main effect of this chemical is to trigger the death of the root sys- tem. To understand the response of root cell membrane lipids to catechin stress, we used the lipidomics approach to study the profiles of Arabidopsis root lipids molecules under catechin treatment. The changes of molecular species in membrane lipids, content of membrane lipids, double bond index （DBI） and acyl chain carbon number of the fatty acid were examined in Wild type （WS） and PLDδ deficient mutant （PLDδ-KO） during catechin treatment. The re- sults indicated that after 90 min treatment with catechin, the lipid contents of digalactosyldiacylglycerol （DGDG） , monogalactosyldiaeylglyeerol （MGDG） , phosphatidylglycerol （PG）, phosphatidyleholine （PC）, and phosphatidyli- nositol （PI） decreased both in WS and PLDS-KO roots, lipid contents of phosphatidylethanolamine （PE） and phos- phatidyfinositol （PS） decreased in WS roots, but increase in PLDδ-KO roots, lipid contents of （phosphatidic acid） PA increased at the begin of treatment and declined to the level of control in WS roots. The ratio of the two major lipids in roots, PC and PE, declined significantly in PLDδ-KO plants, the acyl carbon number of PS in WS plants increased. The results suggested that PLDδ-K0 is more sensitive than WS during catechin treatment, and suppres- sion of PLDδ exacerbated membrane damage induced by catechin.