Benitez-Alfonso Yoselin, Cilia Michelle, San Roman Adrianna, Thomas Carole, Maule Andy, Hearn Stephen, Jackson David
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3615-20. doi: 10.1073/pnas.0808717106. Epub 2009 Feb 13.
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.
植物中的细胞间运输通过称为“胞间连丝”的细胞质通道进行，并受发育和环境因素调控。胼胝质沉积在体内调节胞间连丝运输，但对于调控这一过程的机制知之甚少。在此，我们报道一种鉴定影响胞间连丝运输突变体的遗传学方法。我们分离出5个突变体，命名为绿色荧光蛋白（GFP）转运受阻（gat），这些突变体在GFP从韧皮部卸载到分生组织的过程中受到影响。gat1突变体在幼苗期致死，其在分生组织和器官原基的非绿色质体中表达的m型硫氧还蛋白存在损伤。胼胝质和过氧化氢在gat1突变体中积累，处于氧化条件下的野生型植物表现出与gat1类似的运输缺陷表型。在成熟叶片中异位表达GAT1可增加胞间连丝通透性，并导致衰老和开花时间延迟。我们提出GAT1硫氧还蛋白在胼胝质沉积和共质体通透性的氧化还原调节中发挥作用，这对于拟南芥分生组织的维持至关重要。
