一个受体样激酶在豆科植物适应盐胁迫中的作用

N. Eckardt
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引用次数: 1

摘要

结果表明,盐胁迫能快速诱导根内丝氨酸激酶,而不是甘露醇或低温对丝氨酸激酶的响应。将Srlk启动子与b-葡萄糖醛酸酶标记基因融合的实验表明,盐对根表皮细胞的Srlk表达有强烈的诱导作用。通过RNA干扰(RNAi)和TILLING引入的Srlk突变抑制Srlk,阻止了高盐条件下根生长的抑制(见图)。此外,Srlk突变体植株的钠积累量明显低于对照植株。最后,与对照相比,Srlk突变体中其他几个盐诱导基因在盐胁迫下的诱导水平急剧降低。RLKs具有胞外结构域,通过跨膜结构域连接胞质激酶。植物含有数百种RLKs,这些RLKs被认为在感知环境和发育信号并将这些信号转导给下游效应器方面具有重叠或不同的作用(Morillo和Tax, 2006)。de Lorenzo等人的研究结果表明,Srlk可能在M. truncatula根对盐胁迫的感知以及植物在高盐条件下积累钠的能力中起主要作用。植物对高盐和其他胁迫的反应是高度复杂的,因此通过基因改造提高植物的抗逆性是很困难的(Wang et al., 2003)。确定Srlk的下游信号伙伴和靶基因对盐胁迫的响应和适应具有重要意义。本研究为提高油菜耐盐性开辟了新的研究途径和前景
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A Receptor-Like Kinase That Functions in Adaptation to Salt Stress in Legumes
show that Srlk is rapidly induced by salt stress in M. truncatula roots, rather than in response to mannitol or cold temperature. Experiments with the Srlk-promoter fused to a b-glucuronidase marker gene showed that Srlk expression is strongly induced in root epidermal cells in response to salt. Repression of Srlk using RNA interference (RNAi) and mutations of Srlk introduced through TILLING prevented the inhibition of root growth under high salt conditions (see figure). In addition, Srlk mutant plants were found to accumulate significantly less sodium than control plants. Finally, several other salt-induced genes showed drastically reduced levels of induction following salt stress in the Srlk mutants relative to controls. RLKs possess an extracellular domain connected via a transmembrane domain to a cytoplasmic kinase. Plants contain hundreds of RLKs, which are thought to have overlapping or distinct roles in perceiving environmental and developmental signals and transducing these signals to downstream effectors (reviewed in Morillo and Tax, 2006). The results of de Lorenzo et al. suggest that Srlk may play a primary role in the perception of salt stress by M. truncatula roots and the ability of the plant to accumulate sodium under high salt conditions. Plant response to high salt and other stresses is highly complex, making genetic modification of plants for improved stress tolerance difficult to achieve (Wang et al., 2003). It will be important to identify downstream signaling partners and target genes of Srlk in the response and adaptation to salt stress. This work opens a new pathway for investigation and enhanced prospects for the development of improved salt tolerance in
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