Oligochitosan induces programmed cell death in tobacco suspension cells

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• 作者：Hongyan Zhang^a ; ^b ; Wenxia Wang^a ; Heng Yin^a ; Xiaoming Zhao^a ; ^{zhaoxm@dicp.ac.cn} ; Yuguang Du^a ; ^{dyguang@gmail.com}
• 关键词：Oligochitosan ; PCD ; Ca2+ ; NO ; H2O2 ; Cytochrome c
• 刊名：Carbohydrate Polymers
• 出版年：2012
• 出版时间：14 February, 2012
• 年：2012
• 卷：87
• 期：3
• 页码：2270-2278
• 全文大小：1285 K

文摘

Oligochitosan has been proved to trigger plant cell death. To gain some insights into the mechanisms of oligochitosan-induced cell death, the nature of oligochitosan-induced cell death and the role of calcium (Ca²⁺), nitric oxide (NO) and hydrogen peroxide (H₂O₂) were studied in tobacco suspension cells. Oligochitosan-induced cell death occurred in cytoplasmic shrinkage, phosphatidylserine externalization, chromatin condensation, TUNEL-positive nuclei, cytochrome c release and induction of programmed cell death (PCD)-related gene hsr203J, suggesting the activation of PCD pathway. Pretreatment cells with cyclosporin A, resulted in reducing oligochitosan-induced cytochrome c release and cell death, indicating oligochitosan-induced PCD was mediated by cytochrome c. In the early stage, cells undergoing PCD showed an immediate burst in free cytosolic Ca²⁺ ([Ca²⁺]_cyt) elevation, NO and H₂O₂ production. Further study showed that these three signals were involved in oligochitosan-induced PCD, while Ca²⁺ and NO played a negative role in this process by modulating cytochrome c release.