抗凋亡基因（CED-9）提高植株對鹽脅迫和氧化應激的耐受性
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| 抗凋亡基因（CED-9）提高植株對鹽脅迫和氧化應激的耐受性
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  圖注：Control（圓形）、PVX-WT（三角形）和PVX/CED-9轉基因（方形）煙草植株葉片，在H2O2處理前后，三種葉肉細胞的K+（左）和H+（右）離子流的變化。負值表示離子外流，正值表示離子內流。 凋亡(Apoptosis)是細胞程序性死亡的一種，在調節植物對環境的適應性中起到重要作用。近期有研究表明動物的抗凋亡基因(CED-9)在植物中表達，能夠顯著提高植物對各種生物和非生物脅迫的耐受性，但隱藏在該現象下的最基本的細胞機制尚未被考察。 煙草（Nicotiana benthamiana）瞬時表達了CED-9抗凋亡基因后，對鹽脅迫及氧化應激時植株的特定離子流“指紋”進行了研究。使用非損傷微測技術(MIFE)對離子流進行檢測，可以看到CED-9基因通過改變跨膜K+和H+離子流的模式來提高植株對鹽脅迫和氧化應激的耐受性。 本文首次對植物的“離子流指紋”和細胞程序性死亡機制的關系進行研究，發現CED-9基因可以控制葉肉細胞質膜上的兩種K+通道：KOR和NSCC，從而阻止NaCl引起的鹽脅迫葉片的K+外流；同時，CED-9基因表達能顯著降低氧化應激引起的K+外流，維持胞內離子平衡，以減少氧化應激帶來的短期和長期損害。 | |
關鍵詞：離子流(Ion flux), 膜轉運(Membrane transport), 凋亡(Apoptosis), 鹽脅迫(Salinity), 氧化應激(Oxidative stress)
參考文獻：Sergey Shabala, et al. Planta, 2007, 227:189 -197
全文下載：http://www.xuyue.net/xylt/viewthread.php?tid=538&extra=page%3D1
Abstract
Apoptosis, one form of programmed cell death (PCD), plays an important role in mediating plant adaptive responses to the environment. Recent studies suggest that expression of animal anti-apoptotic genes in transgenic plants may signiWcantly improve a plant’s ability to tolerate a variety of biotic and abiotic stresses. The underlying cellular mechanisms of this process remain unexplored. In this study, we investigated speciWc ion Xux “signatures” in Nicotiana benthamiana plants transiently expressing CED-9 anti-apoptotic gene and undergoing salt- and oxidative stresses. Using a range of electrophysiological techniques, we show that expression of CED-9 increased plant salt and oxidative stress tolerance by altering K+ and H+ Xux patterns across the plasma membrane. Our data shows that PVX/CED-9 plants are capable of preventing stress-induced K+ eZux from mesophyll cells, so maintaining intracellular K+ homeostasis. We attribute these eVects to the ability of CED-9 to control at least two types of K+-permeable channels; outward-rectifying depolarization-activating K+ channels (KOR) and non-selective cation channels (NSCC). A possible scenario linking CED-9 expression and ionic relations in plant cell is suggested. To the best of our knowledge, this study is the Wrst to link “ion Xux signatures” and mechanisms involved in regulation of PCD in plants.
Apoptosis, one form of programmed cell death (PCD), plays an important role in mediating plant adaptive responses to the environment. Recent studies suggest that expression of animal anti-apoptotic genes in transgenic plants may signiWcantly improve a plant’s ability to tolerate a variety of biotic and abiotic stresses. The underlying cellular mechanisms of this process remain unexplored. In this study, we investigated speciWc ion Xux “signatures” in Nicotiana benthamiana plants transiently expressing CED-9 anti-apoptotic gene and undergoing salt- and oxidative stresses. Using a range of electrophysiological techniques, we show that expression of CED-9 increased plant salt and oxidative stress tolerance by altering K+ and H+ Xux patterns across the plasma membrane. Our data shows that PVX/CED-9 plants are capable of preventing stress-induced K+ eZux from mesophyll cells, so maintaining intracellular K+ homeostasis. We attribute these eVects to the ability of CED-9 to control at least two types of K+-permeable channels; outward-rectifying depolarization-activating K+ channels (KOR) and non-selective cation channels (NSCC). A possible scenario linking CED-9 expression and ionic relations in plant cell is suggested. To the best of our knowledge, this study is the Wrst to link “ion Xux signatures” and mechanisms involved in regulation of PCD in plants.
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