Pagliari Laura, Buoso Sara, Santi Simonetta, Furch Alexandra C U, Martini Marta, Degola Francesca, Loschi Alberto, van Bel Aart J E, Musetti Rita
Department of Agricultural, Food, Environmental and Animal Sciences, University of Udine, via delle Scienze, 206, I-33100 Udine, Italy.
Institute of General Botany and Plant Physiology, Friedrich-Schiller-University of Jena, Dornburgerstrasse, 159 D-07743 Jena, Germany.
J Exp Bot. 2017 Jun 15;68(13):3673-3688. doi: 10.1093/jxb/erx199.
In Fabaceae, dispersion of forisomes-highly ordered aggregates of sieve element proteins-in response to phytoplasma infection was proposed to limit phloem mass flow and, hence, prevent pathogen spread. In this study, the involvement of filamentous sieve element proteins in the containment of phytoplasmas was investigated in non-Fabaceae plants. Healthy and infected Arabidopsis plants lacking one or two genes related to sieve element filament formation-AtSEOR1 (At3g01680), AtSEOR2 (At3g01670), and AtPP2-A1 (At4g19840)-were analysed. TEM images revealed that phytoplasma infection induces phloem protein filament formation in both the wild-type and mutant lines. This result suggests that, in contrast to previous hypotheses, sieve element filaments can be produced independently of AtSEOR1 and AtSEOR2 genes. Filament presence was accompanied by a compensatory overexpression of sieve element protein genes in infected mutant lines in comparison with wild-type lines. No correlation was found between phloem mass flow limitation and phytoplasma titre, which suggests that sieve element proteins are involved in defence mechanisms other than mechanical limitation of the pathogen.
在豆科植物中,有人提出,响应植原体感染,筛管分子蛋白的高度有序聚集体——成束收缩蛋白(forisomes)的分散作用可限制韧皮部物质流动,从而防止病原体传播。在本研究中,我们在非豆科植物中研究了丝状筛管分子蛋白在遏制植原体方面的作用。我们分析了缺失一个或两个与筛管分子丝形成相关基因(AtSEOR1(At3g01680)、AtSEOR2(At3g01670)和AtPP2 - A1(At4g19840))的健康和感染拟南芥植株。透射电镜图像显示,植原体感染在野生型和突变株系中均诱导了韧皮部蛋白丝的形成。这一结果表明,与之前的假设相反,筛管分子丝可以独立于AtSEOR1和AtSEOR2基因产生。与野生型株系相比,感染突变株系中丝状结构的存在伴随着筛管分子蛋白基因的补偿性过表达。在韧皮部物质流动限制与植原体滴度之间未发现相关性,这表明筛管分子蛋白参与了除对病原体的机械限制之外的防御机制。