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豌豆种子传播花叶病毒基因组连接蛋白VPg在豌豆致病型特异性毒力后的突变

Mutations in pea seedborne mosaic virus genome-linked protein VPg after pathotype-specific virulence in Pisum sativum.

作者信息

Borgstrøm B, Johansen I E

机构信息

Biotechnology Group, Danish Institute of Agricultural Sciences, Fredriksberg.

出版信息

Mol Plant Microbe Interact. 2001 Jun;14(6):707-14. doi: 10.1094/MPMI.2001.14.6.707.

DOI:10.1094/MPMI.2001.14.6.707
PMID:11386366
Abstract

Pisum sativum plant introduction (PI) line 269818 is resistant to potyvirus pea seedborne mosaic virus (PSbMV) isolates, categorized as pathotype P1, and is susceptible to pathotype P4 isolates. This difference in infectivity is determined by the viral genome-linked protein (VPg) cistron. Mutational analysis of VPg of PSbMV isolates DPD1 and NY representing pathotypes P1 and P4 revealed that codon changes affecting amino acids 105 to 117 in the central region of VPg influenced virulence on PI 269818. In contrast, infectivity on pea cultivar Dark Skinned Perfection, which is susceptible to both pathotypes, was not affected by the mutations. Mutants overcoming resistance in PI 269818 were analyzed for changes in the VPg coding region upon passage through PI 269818 and Dark Skinned Perfection. Adaptive changes were observed only upon passage through PI 269818 and only at codons from amino acid 105 to 117. Expression of DPD1 VPg in PI 269818 did not affect infection by NY, which suggests that VPg from DPD1 is not an elicitor of a general resistance response. The results are compatible with the hypothesis that viral amplification depends upon the interaction between VPg and a host factor.

摘要

豌豆(Pisum sativum)植物引进(PI)品系269818对马铃薯Y病毒属的豌豆种传花叶病毒(PSbMV)分离株具有抗性,这些分离株被归类为致病型P1,而对致病型P4分离株敏感。这种感染性差异由病毒基因组连接蛋白(VPg)顺反子决定。对代表致病型P1和P4的PSbMV分离株DPD1和NY的VPg进行突变分析发现,影响VPg中央区域第105至117位氨基酸的密码子变化影响了对PI 269818的毒力。相比之下,对两种致病型均敏感的豌豆品种深色完美(Dark Skinned Perfection)的感染性不受这些突变影响。分析了在通过PI 269818和深色完美品种后克服PI 269818抗性的突变体VPg编码区的变化。仅在通过PI 269818时且仅在第105至117位氨基酸的密码子处观察到适应性变化。在PI 269818中表达DPD1 VPg不影响NY的感染,这表明来自DPD1的VPg不是一般抗性反应的激发子。这些结果与病毒扩增取决于VPg与宿主因子之间相互作用的假说相符。

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