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拟南芥双突变体叶片中的糖分积累增强了水杨酸介导的防御反应的启动。

Sugar Accumulation in Leaves of Arabidopsis Double Mutants Enhances Priming of the Salicylic Acid-Mediated Defense Response.

作者信息

Gebauer Pierre, Korn Martin, Engelsdorf Timo, Sonnewald Uwe, Koch Christian, Voll Lars M

机构信息

Division of Biochemistry, Friedrich-Alexander-Universität Erlangen-NürnbergErlangen, Germany.

出版信息

Front Plant Sci. 2017 Aug 8;8:1378. doi: 10.3389/fpls.2017.01378. eCollection 2017.

DOI:10.3389/fpls.2017.01378
PMID:28848581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5550771/
Abstract

In compatible interactions, biotrophic microbial phytopathogens rely on the supply of assimilates by the colonized host tissue. It has been found in rice that phloem localized SWEET sucrose transporters can be reprogrammed by bacterial effectors to establish compatibility. We observed that / double mutants, but not single mutants, exhibited increased resistance toward the fungal hemibiotroph (), both in the biotrophic and the necrotrophic colonization phase. We therefore investigated if the phloem localized transporters SWEET11 and SWEET12 represent additive susceptibility factors in the interaction of Arabidopsis with . SWEET12-YFP fusion protein driven by the endogenous promoter strongly accumulated at infection sites and in the vasculature upon challenge with . However, susceptibility of single mutants to was comparable to wild type, indicating that the accumulation of SWEET12 at infection sites does not play a major role for compatibility. SWEET12-YFP reporter protein was not detectable at the plant-pathogen interface, suggesting that is not targeted by effectors. SWEET11-YFP accumulation in plants were similar in infected and mock control leaves. A close inspection of major carbohydrate metabolism in non-infected control plants revealed that soluble sugar and starch content were substantially elevated in / double mutants during the entire diurnal cycle, that diurnal soluble sugar turnover was increased more than twofold in /, and that accumulation of free hexoses and sucrose was strongly expedited in double mutant leaves compared to wild type and both single mutants during the course of infection. After 2 days of treatment, free and conjugated SA levels were significantly increased in infected and mock control leaves of / relative to all other genotypes, respectively. Induced genes in mock treated / leaves were highly significantly enriched for several GO terms associated with SA signaling and response compared to mock treated wild-type leaves, indicating sugar-mediated priming of the SA pathway in the double mutant. Infection assays with salicylic acid deficient / triple mutants demonstrated that reduced susceptibility observed in / was entirely dependent on the SA pathway. We suggest a model how defects in phloem loading of sucrose can influence SA priming and hence, compatibility.

摘要

在亲和性互作中,活体营养型微生物植物病原菌依赖于被侵染的宿主组织提供同化物。在水稻中发现,韧皮部定位的SWEET蔗糖转运蛋白可被细菌效应子重新编程以建立亲和性。我们观察到,在活体营养和死体营养定殖阶段,双突变体而非单突变体对真菌半活体营养菌()表现出增强的抗性。因此,我们研究了韧皮部定位的转运蛋白SWEET11和SWEET12在拟南芥与的互作中是否代表累加的感病因子。由内源启动子驱动的SWEET12 - YFP融合蛋白在用挑战后在感染位点和维管系统中强烈积累。然而,单突变体对的感病性与野生型相当,这表明SWEET12在感染位点的积累对亲和性不起主要作用。在植物 - 病原体界面未检测到SWEET12 - YFP报告蛋白,这表明不被效应子靶向。在感染和模拟对照叶片中,植物中SWEET11 - YFP的积累相似。对未感染的对照植物中主要碳水化合物代谢的仔细检查发现,在整个昼夜周期中,/双突变体中的可溶性糖和淀粉含量大幅升高,在/中昼夜可溶性糖周转率增加了两倍多,并且在感染过程中,与野生型和两个单突变体相比,双突变体叶片中游离己糖和蔗糖的积累强烈加快。处理2天后,与所有其他基因型相比,/感染和模拟对照叶片中的游离和结合SA水平分别显著增加。与模拟处理的野生型叶片相比,模拟处理的/叶片中的诱导基因在与SA信号传导和反应相关的几个GO术语中高度显著富集,表明双突变体中糖介导的SA途径的启动。用缺乏水杨酸的/三突变体进行的感染试验表明,在/中观察到的感病性降低完全依赖于SA途径。我们提出了一个模型,说明蔗糖韧皮部装载缺陷如何影响SA启动,进而影响亲和性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/d29ae79f89a9/fpls-08-01378-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/6251578c07b8/fpls-08-01378-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/bd1b9a4ad4c2/fpls-08-01378-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/dccc573f94b2/fpls-08-01378-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/01ac6787a629/fpls-08-01378-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/c6cd2abc069a/fpls-08-01378-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/d29ae79f89a9/fpls-08-01378-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/6251578c07b8/fpls-08-01378-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/bd1b9a4ad4c2/fpls-08-01378-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/dccc573f94b2/fpls-08-01378-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/01ac6787a629/fpls-08-01378-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/c6cd2abc069a/fpls-08-01378-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/083c/5550771/d29ae79f89a9/fpls-08-01378-g006.jpg

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