2-烯醛还原酶基因（AER）在提高植物抗旱抗盐中的作用和机理

Reactive oxygen species (ROS) production increases in plants under environmental stresses. The excessive ROS damage cell directly, which caused the upstream of oxidative damage. ROS attack the important component of cell membrane―polyunsaturated fatty acids (PUFAs), causes chain reaction of lipid peroxidation and produces plenty of reactive aldehyde radicals. These reactive aldehyde radicals, which formed downstream of ROS production are more harmful than ROS and they further damage cell seriously. A lot of studies have been done related to the upstream of oxidative damage (that is ROS toxicity), while little is known about the downstream (that is aldehyde toxicity), because it is rather difficult to separate upstream and downstream of oxidative damage. In this study, we use 2-alkenal reduactase (AER) overexpression tobacco, which only scavenges lipid peroxidation―derived aldehydes but has no effect on ROS production, thus can clearly separate the upstream and downstream of oxidative damage, investigate whether aldehyde toxicity is involved in drought and salt-induced plant damage. At the same time, identify the aldehyde species and content under drought and salt stress, and clarify the mechanism of AER in drought and salt resistance. Furthermore, the important antioxidant enzymes in plants―superoxide dismutase (SOD) and catalase (CAT) genes will be introduced into AER overexpression tobacco, to produce double genes overexpression plant materials. Using these special materials, we will study the effect of alleviation of upstream, downstream and the whole oxidative damage on drought and salt resistance, illustrate the relationship between upstream and downstream of oxidative damage under drought and salt stress. This study will clarify whether aldehydes are involved in drought and salt stress, and whether scavenge of aldehydes can result in enhanced drought and salt resistance. The result of this study could contribute to a better understand of oxidative damage and provide a new strategy for improving drought and salt resistance in plants.

环境胁迫产生过量的活性氧，攻击细胞膜组分多聚不饱和脂肪酸，继而引发脂质过氧化链式反应并产生大量的活性醛基，活性醛基进一步引起细胞伤害，构成氧化伤害的下游。过去研究较多的是氧化伤害的上游即活性氧伤害，而对氧化伤害下游醛的伤害，受研究手段限制，了解不多。本研究以超表达2-烯醛还原酶基因（AER）烟草为材料，利用其可以区分活性氧上、下游伤害的特点，即只清除醛类物质，而对活性氧的累积没有影响，以活性氧下游伤害为重点研究对象，研究醛毒害是否参与了干旱和盐胁迫对植物的伤害，并鉴定醛基种类和水平，明确AER在抗旱和抗盐中的作用机制。此外，本研究将把抗氧化酶SOD、CAT，和AER一起转入到烟草中，构建转双基因植物材料，比较清除氧化伤害上游、下游和整个氧化伤害系统对干旱和盐害的反应，明确抗氧化上、下游的关系。通过完成本研究，将明确醛是否参与了干旱和盐胁迫，验证是否可以通过清除醛基来提高植物的抗旱和抗盐能力

干旱和盐害等逆境胁迫所引起的氧化伤害是造成植物生长发育缓慢、作物产量下降的重要原因之一。植物的氧化伤害可分为两个阶段，即上游的活性氧伤害和下游的醛基伤害。以往的研究对上游的活性氧的伤害关注的较多，而对醛基伤害探索的较少。本项目利用2-烯醛还原酶（AER）对氧化伤害下游所产生的醛类物质的有效清除作用，围绕AER基因提高植物抗旱和抗盐的能力的作用和机理开展了相关的研究。结果表明，醛类物质的累积是干旱或者盐胁迫引起的植物细胞氧化伤害的重要原因之一；超表达AER基因可以显著提高植株在干旱或者盐胁迫下的抗氧化能力，维持叶片较高的叶绿素含量和较高的光合能力，并减少丙二醛的累积，从而有效提高了植物的抗旱和抗盐能力。同时，我们还创造了转双基因的植物材料，即同时超表达抗氧化基因和AER基因，并验证了转双基因和转单基因植物材料对提高植物抗旱和抗盐能力的异同。我们发现，转双基因的植株比野生型具有较高的生物量和光合能力以及较少的活性氧和丙二醛的累积，说明其具有较强的抗旱和抗盐能力。但是与转单基因的植株相比，转双基因的植株并没有表现出更强的生长能力和抗氧化能力，说明转双基因植株并没有获得比转单基因的植株更强的抗旱和抗盐能力。上述研究阐明了AER与植物抗旱和抗盐性的关系，为提高植物抗旱抗盐能力提供了一种新的途径，也为培育抗旱和抗盐的作物品种提供了一种新的研究思路和依据。.