Crosstalk among nitric oxide, calcium and reactive oxygen species during triterpenoid biosynthesis in Betula platyphylla

被引:6
|
作者
Zeng, Fansuo [1 ,2 ]
Liu, Kun [2 ]
Li, Sida [2 ]
Zhan, Yaguang [1 ,2 ]
机构
[1] Northeast Forestry Univ, State Key Lab Tree Genet & Breeding, Harbin 150040, Peoples R China
[2] Northeast Forestry Univ, Coll Life Sci, Harbin 150040, Peoples R China
基金
中国国家自然科学基金;
关键词
apoptosis; Ca2+; cell death; enzymes; oxidative stress; white birch; PROGRAMMED CELL-DEATH; CHINENSIS VAR. MAIREI; ISOPRENOID BIOSYNTHESIS; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; SUSPENSION-CULTURES; TAXOL PRODUCTION; OXIDATIVE BURST; NADPH OXIDASE; GROWTH;
D O I
10.1071/FP14352
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
We analysed NO, reactive oxygen species (ROS) and Ca2+ crosstalk during triterpenoid biosynthesis in white birch (Betula platyphylla Suk.) cells. Cells were pretreated with diphenyleneiodonium, sodium diethyldithiocarbamate (DDTC) or catalase (CAT), or a Ca2+ channel blocker or chelator before sodium nitroprusside treatment. Changes in triterpenoid, malondialdehyde and proline levels, cell viability, and CAT, ascorbate peroxidase and peroxidase activity were recorded. Furthermore, enzyme gene expression levels related to triterpene biosynthesis, endogenous signalling and antioxidase activity, and cell apoptosis and death rates were measured. Sodium nitroprusside elevated ROS and Ca2+ levels. Oleanolic acid levels in cells pretreated with diphenyleneiodonium and CAT reduced significantly, but it increased with DDTC pretreatment. ROS inhibition downregulated BpDXR, BpCALM and BpNIA expression. Oleanolic acid, BpMnSOD expression, and CAT, ascorbate peroxidase and peroxidase activities reduced when the Ca2+ signalling pathway was blocked. The apoptosis rates of cells pretreated with DDTC and CAT decreased significantly; cell death rates also reduced in groups Ca2+ pretreated with channel blocker and chelator . Thus ROS and Ca2+ participate in triterpenoid biosynthesis, cell apoptosis and death induced by exogenous NO application. Further, NO causes oxidative stress and restricts the level of intracellular ROS through the Ca2+ signalling pathway.
引用
收藏
页码:643 / 654
页数:12
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