Keller K E, Johansen I E, Martin R R, Hampton R O
USDA-ARS, Horticultural Crops Research Laboratory, Oregon State University, Corvallis 97330, USA.
Mol Plant Microbe Interact. 1998 Feb;11(2):124-30. doi: 10.1094/MPMI.1998.11.2.124.
The mechanism of Pisum sativum pathotype-specific resistance to pea seed-borne mosaic potyvirus (PSbMV) was investigated and the coding region determinant of PSbMV virulence was defined. Homozygous recessive sbm-1 peas are unable to support replication of PSbMV pathotype 1 (P-1), whereas biochemically and serologically related pathotype 4 (P-4) is fully infectious in the sbm-1/sbm-1 genotype. We were unable to detect viral coat protein or RNA with double antibody sandwich-enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction in sbm-1/sbm-1 P-1-inoculated protoplasts and plants. Lack of viral coat protein or RNA in P-1 transfected sbm-1/sbm-1 protoplasts suggests that sbm-1 resistance is occurring at the cellular level and that inhibition of cell-to-cell virus movement is not the operating form of resistance. In addition, because virus products were not detected at any time post-inoculation, resistance must either be constitutive or expressed very early in the virus infection process. P-1-resistant peas challenged with full-length, infectious P-1/P-4 recombinant clones demonstrated that a specific P-4 coding region, the 21-kDa, genome-linked protein (VPg), was capable of overcoming sbm-1 resistance, whereas clones containing the P-1 VPg coding region were noninfectious to sbm-1/sbm-1 peas. VPg is believed to be involved in potyvirus replication and its identification as the PSbMV determinant of infectivity in sbm-1/sbm-1 peas is consistent with disruption of an early P-1 replication event.
研究了豌豆对豌豆种传花叶马铃薯Y病毒（PSbMV）致病型特异性抗性的机制，并确定了PSbMV毒力的编码区决定因素。纯合隐性sbm-1豌豆无法支持PSbMV致病型1（P-1）的复制，而在生化和血清学上相关的致病型4（P-4）在sbm-1/sbm-1基因型中具有完全感染性。我们无法通过双抗体夹心酶联免疫吸附测定和逆转录-聚合酶链反应在接种了P-1的sbm-1/sbm-1原生质体和植物中检测到病毒外壳蛋白或RNA。在转染了P-1的sbm-1/sbm-1原生质体中缺乏病毒外壳蛋白或RNA，这表明sbm-1抗性发生在细胞水平，并且细胞间病毒运动的抑制不是抗性的作用形式。此外，由于在接种后的任何时间都未检测到病毒产物，抗性要么是组成型的，要么在病毒感染过程的早期就表达。用全长感染性P-1/P-4重组克隆挑战P-1抗性豌豆，结果表明一个特定的P-4编码区，即21 kDa的基因组连接蛋白（VPg），能够克服sbm-1抗性，而含有P-1 VPg编码区的克隆对sbm-1/sbm-1豌豆无感染性。VPg被认为参与马铃薯Y病毒的复制，其作为sbm-1/sbm-1豌豆中PSbMV感染性决定因素的鉴定与早期P-1复制事件的破坏一致。
