Identification of amino acids of the beet necrotic yellow vein virus p25 protein required for induction of the resistance response in leaves of Beta vulgaris plants
Identification of amino acids of the beet necrotic yellow vein virus p25 protein required for induction of the resistance response in leaves of Beta vulgaris plants
复制标题
DOI：
10.1099/vir.0.83624-0
复制
发表时间：
2008-05-01
影响因子：
3.8
通讯作者：
Tamada, Tetsuo
中科院分区：
文献类型：
--
作者：
Chiba, Soutaro;Miyanishi, Masaki;Tamada, Tetsuo
甜菜坏死黄静脉病毒（BNYVV）的rna3编码p25蛋白与甜菜根（Beta vulgaris subsp）的根瘤症状有关。寻常的)。本研究发现，p25蛋白的存在也与甜菜和野生甜菜（Beta vulgaris subsp）摩擦接种叶片的抗性反应有关。maritima)植物。抗性表型表现出一系列症状，从没有可见的病变到接种部位的坏死或灰色病变，只有非常低水平的病毒和病毒RNA积累。易感表型表现为大的亮黄色病变，并发展为高水平的病毒积聚。然而，在多粘菌载体接种后的根中，除了感染的早期阶段外，在易感和抗性表型的植物之间，病毒和病毒RNA积累水平没有明显差异。BNYVV菌株与两个选定的野生甜菜品系（MR1和MR2）和甜菜品种之间存在基因型特异性互作。对天然BNYVV分离株的序列分析和p25蛋白的定点诱变表明，位于第68、70和179位的3个aa残基对抗性表型有重要影响，宿主基因型特异性受第68位单氨基酸变化的控制。讨论了BNYVV耐药菌株发生的机理。
The RNA3-encoded p25 protein of beet necrotic yellow vein virus (BNYVV) is responsible for the production of rhizomania symptoms of sugar beet roots (Beta vulgaris subsp. vulgaris). Here, it was found that the presence of the p25 protein is also associated with the resistance response in rub-inoculated leaves of sugar beet and wild beet (Beta vulgaris subsp. maritima) plants. The resistance phenotype displayed a range of symptoms from no visible lesions to necrotic or greyish lesions at the inoculation site, and only very low levels of virus and viral RNA accumulated. The susceptible phenotype showed large, bright yellow lesions and developed high levels of virus accumulation. In roots after Polymyxa betae vector inoculation, however, no drastic differences in virus and viral RNA accumulation levels were found between plants with susceptible and resistant phenotypes, except at an early stage of infection. There was a genotype-specific interaction between BNYVV strains and two selected wild beet lines (MR1 and MR2) and sugar beet cultivars. Sequence analysis of natural BNYVV isolates and site-directed mutagenesis of the p25 protein revealed that 3 aa residues at positions 68, 70 and 179 are important in determining the resistance phenotype, and that host-genotype specificity is controlled by single amino acid changes at position 68. The mechanism of the occurrence of resistance-breaking BNYVV strains is discussed.