Ogawa T, Watanabe Y, Meshi T, Okada Y
Tochigi Laboratory, P.C.C. Technology Inc., Tochigi Prefecture, Japan.
Virology. 1991 Dec;185(2):580-4. doi: 10.1016/0042-6822(91)90528-j.
We examined whether the 130K and 180K proteins of tobacco mosaic virus (TMV), the putative virus-encoded replicase components, produced by a replication-competent TMV mutant could complement a replication-defective mutant in a single cell. The replication-competent mutant (LDCS29) had a deletion in the coat protein gene and the replication-defective mutant (LDR28) had a large deletion in the gene encoding the 130K and 180K proteins. Neither the replication of LDR28 nor the production of the coat protein from LDR28 or LDCS29 was detected when the mutants were inoculated separately into tobacco protoplasts. However, when the two mutants were co-inoculated, the production of the LDR28 genomic RNA and the subgenomic RNA for the coat protein and accumulation of the coat protein were observed. These results show that the virus-encoded replicase components of TMV complemented the replication-defective mutant in trans.
我们研究了烟草花叶病毒(TMV)的130K和180K蛋白(推测为病毒编码的复制酶组分),由一个具有复制能力的TMV突变体产生的这些蛋白,是否能在单个细胞中互补一个复制缺陷型突变体。具有复制能力的突变体(LDCS29)在外壳蛋白基因中有一个缺失,而复制缺陷型突变体(LDR28)在编码130K和180K蛋白的基因中有一个大的缺失。当将这些突变体分别接种到烟草原生质体中时,未检测到LDR28的复制,也未检测到LDR28或LDCS29产生外壳蛋白。然而,当将这两个突变体共同接种时,观察到了LDR28基因组RNA和外壳蛋白亚基因组RNA的产生以及外壳蛋白的积累。这些结果表明,TMV的病毒编码复制酶组分在反式作用中互补了复制缺陷型突变体。