Role of calcium in nitric oxide-induced programmed cell death in tobacco protoplasts

被引：13
作者：
Wang, Y. [1 ,2 ]
Lin, J. S. [2 ]
Wang, G. X. [3 ]
机构：
[1] Dalian Fisheries Univ, Key Lab Hydrobiol Liaoning Prov Univ, Dalian 116023, Liaoning Prov, Peoples R China
[2] Lanzhou Univ, Minist Educ, Key Lab Arid Agroecol, Lanzhou 730000, Gansu Province, Peoples R China
[3] Zhejiang Univ, Coll Life Sci, Hangzhou 310029, Zhejiang, Peoples R China
来源：
BIOLOGIA PLANTARUM | 2010年 / 54卷 / 03期
关键词：
mitochondria; mitochondrial permeability transition; sodium nitroprusside; MITOCHONDRIAL PERMEABILITY TRANSITION; PLANT-CELLS; CA2+; APOPTOSIS; STRESS; ARABIDOPSIS; INVOLVEMENT; SUSPENSION; PATHWAYS; CULTURES;
D O I：
10.1007/s10535-010-0083-2
中图分类号：
Q94 [植物学];
学科分类号：
071001 ;
摘要：
We tried to determine the mechanisms by which Ca(2+) mediated NO-induced programmed cell death (PCD) in tobacco protoplasts. Treatment of tobacco protoplasts with the NO donor sodium nitroprusside (SNP) resulted in a rapid [Ca(2+)](cyt) accumulation and decrease in mitochondrial membrane potential (Delta I(m)) before the appearance of PCD. NO-induced PCD could be largely prevented not only by NO scavenger c-PTIO, but also by EGTA (Ca(2+) chelator), LaCl(3) (Ca(2+)-channel blocker) or CsA (a specific mitochondrial permeability transition pore inhibitor, which also inhibit Ca(2+) cycling by mitochondria). All results suggested that NO-induced PCD is mediated through mitochondrial pathway and regulated by Ca(2+).
引用
收藏
页码：471 / 476
页数：6
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