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首页> 外文期刊>Molecular Plant-Microbe Interactions >Novel Secretory Protein Ss-Caf1 of the Plant-Pathogenic Fungus Sclerotinia sclerotiorum Is Required for Host Penetration and Normal Sclerotial Development
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Novel Secretory Protein Ss-Caf1 of the Plant-Pathogenic Fungus Sclerotinia sclerotiorum Is Required for Host Penetration and Normal Sclerotial Development

机译:植物病原性真菌菌核盘菌的新型分泌蛋白Ss-Caf1是宿主穿透和正常菌核发育所必需的。

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To decipher the mechanism of pathogenicity in Sclerotinia sclerotiorum, a pathogenicity-defective mutant, Sunf-MT6, was isolated from a T-DNA insertional library. Sunf-MT6 could not form compound appressorium and failed to induce lesions on leaves of rapeseed though it could produce more oxalic acid than the wild-type strain. However, it could enter into host tissues via wounds and cause typical necrotic lesions. Furthermore, Sunf-MT6 produced fewer but larger sclerotia than the wild-type strain Sunf-M. A gene, named Ss-caf1, was disrupted by T-DNA insertion in Sunf-MT6. Gene complementation and knockdown experiments confirmed that the disruption of Ss-caf1 was responsible for the phenotypic changes of Sunf-MT6. Ss-caf1 encodes a secretory protein with a putative Ca2+-binding EF-hand motif. High expression levels of Ss-caf1 were observed at an early stage of compound appressorium formation and in immature sclerotia. Expression of Ss-caf1 without signal peptides in Nicotiana benthamiana via Tobacco rattle virus-based vectors elicited cell death. These results suggest that Ss-caf1 plays an important role in compound appressorium formation and sclerotial development of S. sclerotiorum. In addition, Ss-Caf1 has the potential to interact with certain host proteins or unknown substances in host cells, resulting in subsequent host cell death.
机译:为了解释核盘菌的致病机理,从T-DNA插入文库中分离出一种致病性缺陷突变体Sunf-MT6。尽管Sunf-MT6可以产生比野生型菌株更多的草酸,但它不能形成复合膜并且不能诱导油菜籽叶上的损伤。但是,它可能通过伤口进入宿主组织并引起典型的坏死性病变。此外,Sunf-MT6产生的菌核少于野生型Sunf-M。一个名为Ss-caf1的基因被Sunf-MT6中的T-DNA插入破坏。基因互补和敲除实验证实,Ss-caf1的破坏是Sunf-MT6的表型变化的原因。 Ss-caf1编码具有假定的Ca2 +结合EF手基序的分泌蛋白。 Ss-caf1的高表达水平观察到复合Appressorium形成的早期和未成熟的菌核。 Ss-caf1不表达信号肽的烟草中通过基于烟草拨浪鼓病毒的载体在本氏烟草中引起细胞死亡。这些结果表明,Ss-caf1在S.sclerotiorum的复合膜形成和硬化发育中起重要作用。此外,Ss-Caf1可能与宿主细胞中的某些宿主蛋白或未知物质发生相互作用,从而导致随后的宿主细胞死亡。

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