THE BARLEY STRIPE MOSAIC-VIRUS GAMMA-B GENE ENCODES A MULTIFUNCTIONAL CYSTEINE-RICH PROTEIN THAT AFFECTS PATHOGENESIS
THE BARLEY STRIPE MOSAIC-VIRUS GAMMA-B GENE ENCODES A MULTIFUNCTIONAL CYSTEINE-RICH PROTEIN THAT AFFECTS PATHOGENESIS
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DOI：
10.1105/tpc.6.11.1593
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发表时间：
1994-11-01
期刊：
影响因子：
11.6
通讯作者：
JACKSON, AO
中科院分区：
文献类型：
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作者：
DONALD, RGK;JACKSON, AO
大麦条纹花叶病毒含有7个基因，其中之一指定一个17 kD的富含半胱氨酸的蛋白质，γ B，这是已知的影响毒力。为了进一步表征γ B在发病机制中的作用，我们诱变编码两个簇内的半胱氨酸和组氨酸残基的富含半胱氨酸的结构域和一组位于簇之间的碱性氨基酸的氨基酸序列，并确定这些突变对大麦症状表型的影响。在簇1中的三个单一氨基酸取代和在碱性区域中的两个氨基酸交换引起与γ B蛋白积累的显著升高相关的漂白症状。相比之下，簇2中的三个单一氨基酸取代和基本基序中的突变导致γ B基因缺失时产生的典型症状减弱（“无效”）。感染了这些“无效"突变体的组织中γ B蛋白的含量略有升高，但外壳蛋白和假定的运动蛋白β B的含量显著降低。遗传互补试验表明，簇1突变是显性的野生型γ B基因，而那些在簇2是隐性的。这些结果突出了γ B在发病机制中的关键作用，并表明这两个富含半胱氨酸的簇在功能上是不同的，它们影响疾病发展的不同方面。
Barley stripe mosaic virus contains seven genes, one of which specifies a 17-kD cysteine-rich protein, gamma b, that is known to affect virulence. To further characterize the role of gamma b in pathogenesis, we mutagenized sequences encoding amino acids within two clusters of cysteine and histidine residues in the cysteine-rich domain and a group of basic amino acids located between the clusters and determined the effects of these mutations on the symptom phenotype in barley. Three single amino acid substitutions in cluster 1 and two amino acid exchanges in the basic region caused bleached symptoms associated with pronounced elevations in accumulation of gamma b protein. In contrast, three single amino acid substitutions in cluster 2 and a mutation in the basic motif resulted in attenuated (''null'') symptoms typical of those produced when the gamma b gene is deleted. Tissue infected with these ''null'' mutants accumulated slightly elevated amounts of the gamma b protein but significantly lower levels of coat protein and the putative movement protein beta b. Genetic complementation tests revealed that cluster 1 mutations are dominant over the wild-type gamma b gene, whereas those in cluster 2 are recessive. These results highlight the pivotal role of gamma b in pathogenesis and suggest that the two cysteine-rich clusters are functionally distinct and that they affect different aspects of disease development.