Biologia plantarum 2010, 54:471-476 | DOI: 10.1007/s10535-010-0083-2
Role of calcium in nitric oxide-induced programmed cell death in tobacco protoplasts
- 1 Key Laboratory of Hydrobiology in Liaoning Province's Universities, Dalian Fisheries University, Dalian, Liaoning Province, P.R. China
- 2 Key Laboratory of Arid Agroecology at Lanzhou University, Ministry of Education, Lanzhou Gansu Province, P.R. China
- 3 College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang Province, P.R. China
We tried to determine the mechanisms by which Ca2+ 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 [Ca2+]cyt accumulation and decrease in mitochondrial membrane potential (ΔΨm) before the appearance of PCD. NO-induced PCD could be largely prevented not only by NO scavenger c-PTIO, but also by EGTA (Ca2+ chelator), LaCl3 (Ca2+-channel blocker) or CsA (a specific mitochondrial permeability transition pore inhibitor, which also inhibit Ca2+ cycling by mitochondria). All results suggested that NO-induced PCD is mediated through mitochondrial pathway and regulated by Ca2+.
Keywords: mitochondria; mitochondrial permeability transition; sodium nitroprusside
Subjects: calcium; Nicotiana tabacum; nitric oxide; programmed cell death; tobacco
Received: August 21, 2008; Accepted: May 5, 2009; Published: September 1, 2010Show citation
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