【作者】 王闻哲； 潘建伟； 郑科； 陈虹； 邵红红； 郭亚娟； 边红武； 韩凝； 王君晖； 朱睦元；

【机构】 浙江大学生命科学学院；

【摘要】 <正>The molecular mechanisms of aluminum(Al)toxicity and tolerance in plants are always the focus of ongoing research in the area of stress phytophysiology.Al toxicity has been extensively studied.Disruption of cytoplasmic Ca2+ homeostasis has been suggested as a primary trigger of Al toxicity.Al causes an increase in cytosolic Ca2+ activity,potentially disrupting numerous biochemical and physiological processes.On the other hand,Al toxicity also elicits the induction of reactive oxygen species(ROS)as well as peroxidative damage to membranes.Al-induced ROS generation and associated mitochondrial dysfunction could be involved in Al inhibition of root growth.Al tolerance in plants has been identified as external exclusion and internal detoxification, and moreover recently a mayor Al-tolerant gene ALMT1(Al-activated malate transporter)has been identified and isolated in some plant species,but detailed molecular mechanisms of Al tolerance are not completely clarified because of its genetically complex nature.Increasing evidence showed that A1 toxicity induces programmed cell death(PCD)in plants,animals and yeast.Our recently published data have revealed that apoptotic suppressors Ced-9,Bcl-2 and PpBI-1 promote the tolerance of yeast cells to Al toxicity.Although regulators of PCD machinery are evolutionarily conserved to some extent in different eukaryotic kingdoms,there is no direct evidence confirming that these apoptotic suppressors inhibit Al-induced PCD in plants and enhance plant tolerance to Al toxicity.Here,we provided substantial evidence showing that C.elegans apoptotic suppressor Ced-9 inhibited Al-or salt-induced programmed cell death(PCD)through downregulation of Al-or salt-induced transcriptional levels of caspase-like vacuolar processing enzyme(VPE)in tobacco,and that Ced-9 significantly enhanced the tolerance of tobacco plants to Al toxicity and salt stress.Our further analyses found that Ced-9 inhibited to a great extent Al-induced expression levels of Al early response genes and decreased intracellular Al accumulation in the root tip.These data clearly suggest that Ced-9 inhibition of Al-induced PCD via downregulation of Al-induced VPE expression leads to promotion of Al tolerance in plants,indicating that negative regulators of plant PCD are involved in integrated regulation of Al tolerance by unknown mechanisms.更多还原

【Abstract】 The molecular mechanisms of aluminum(Al)toxicity and tolerance in plants are always the focus of ongoing research in the area of stress phytophysiology.Al toxicity has been extensively studied.Disruption of cytoplasmic Ca2+ homeostasis has been suggested as a primary trigger of Al toxicity.Al causes an increase in cytosolic Ca2+ activity,potentially disrupting numerous biochemical and physiological processes.On the other hand,Al toxicity also elicits the induction of reactive oxygen species(ROS)as well as peroxidative damage to membranes.Al-induced ROS generation and associated mitochondrial dysfunction could be involved in Al inhibition of root growth.Al tolerance in plants has been identified as external exclusion and internal detoxification, and moreover recently a mayor Al-tolerant gene ALMT1(Al-activated malate transporter)has been identified and isolated in some plant species,but detailed molecular mechanisms of Al tolerance are not completely clarified because of its genetically complex nature.Increasing evidence showed that A1 toxicity induces programmed cell death(PCD)in plants,animals and yeast.Our recently published data have revealed that apoptotic suppressors Ced-9,Bcl-2 and PpBI-1 promote the tolerance of yeast cells to Al toxicity.Although regulators of PCD machinery are evolutionarily conserved to some extent in different eukaryotic kingdoms,there is no direct evidence confirming that these apoptotic suppressors inhibit Al-induced PCD in plants and enhance plant tolerance to Al toxicity.Here,we provided substantial evidence showing that C.elegans apoptotic suppressor Ced-9 inhibited Al-or salt-induced programmed cell death(PCD)through downregulation of Al-or salt-induced transcriptional levels of caspase-like vacuolar processing enzyme(VPE)in tobacco,and that Ced-9 significantly enhanced the tolerance of tobacco plants to Al toxicity and salt stress.Our further analyses found that Ced-9 inhibited to a great extent Al-induced expression levels of Al early response genes and decreased intracellular Al accumulation in the root tip.These data clearly suggest that Ced-9 inhibition of Al-induced PCD via downregulation of Al-induced VPE expression leads to promotion of Al tolerance in plants,indicating that negative regulators of plant PCD are involved in integrated regulation of Al tolerance by unknown mechanisms.更多还原