Control of Arabidopsis meristem development by thioredoxin-dependent regulation of intercellular transport
Control of Arabidopsis meristem development by thioredoxin-dependent regulation of intercellular transport
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DOI：
10.1073/pnas.0808717106
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发表时间：
2009-03-03
影响因子：
11.1
通讯作者：
Jackson, David
中科院分区：
文献类型：
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作者：
Benitez-Alfonso, Yoselin;Cilia, Michelle;Jackson, David
植物细胞间的运输是通过称为“胞间连丝”的细胞质通道进行的，并受发育和环境因素的调节。胼胝质沉积调节胞间连丝的运输在体内，但很少有人知道的机制，调节这一进程。在这里，我们报告了一种遗传方法来确定影响胞间连丝运输的突变体。我们分离到5个突变体，命名为绿色荧光蛋白捕获运输（gat），影响绿色荧光蛋白卸载从韧皮部到分生组织。GAT1突变体是幼苗致死的，并且在分生组织和器官原基的非绿色质体中表达的M型硫氧还蛋白中携带损伤。胼胝质和过氧化氢积累的GAT1突变体，和野生型植物受到氧化条件表型模仿的GAT1贩运缺陷。GAT1在成熟叶片中的异位表达增加了胞间连丝的透性，并导致衰老和开花时间的延迟。我们提出的GAT1硫氧还蛋白在氧化还原调节胼胝质沉积和共质体渗透性，这是至关重要的分生组织的维护在拟南芥中的作用。
Cell-to-cell transport in plants occurs through cytoplasmic channels called "plasmodesmata'' and is regulated by developmental and environmental factors. Callose deposition modulates plasmodesmal transport in vivo, but little is known about the mechanisms that regulate this process. Here we report a genetic approach to identify mutants affecting plasmodesmal transport. We isolated 5 mutants, named gfp arrested trafficking (gat), affected in GFP unloading from the phloem into the meristem. gat1 mutants were seedling lethal and carried lesions in an m-type thioredoxin that is expressed in non-green plastids of meristems and organ primordia. Callose and hydrogen peroxide accumulated in gat1 mutants, and WT plants subjected to oxidative conditions phenocopied the gat1 trafficking defects. Ectopic expression of GAT1 in mature leaves increased plasmodesmal permeability and led to a delay in senescence and flowering time. We propose a role for the GAT1 thioredoxin in the redox regulation of callose deposition and symplastic permeability that is essential for meristem maintenance in Arabidopsis.