Trans complementation of virus-encoded replicase components of tobacco mosaic virus

• Published in: Virology (New York, N.Y.) Vol. 185; no. 2; pp. 580 - 584
• Main Authors: Ogawa, Toshiya, Watanabe, Yuichiro, Meshi, Tetsuo, Okada, Yoshimi
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 01.12.1991; Elsevier
• Subjects: ARN; Biological and medical sciences; Blotting, Northern; Blotting, Western; Capsid - analysis; Capsid - genetics; Chromosome Deletion; Defective Viruses - genetics; Fundamental and applied biological sciences. Psychology; GENE; GENES; Genetic Complementation Test; GENETICA; Genetics; GENETIQUE; GENOMAS; GENOME; Kinetics; Microbiology; MUTANT; MUTANTES; Mutation - genetics; Nicotiana - microbiology; Plants, Toxic; Plasmids - genetics; PROTEINAS; PROTEINE; Protoplasts - microbiology; RNA-Dependent RNA Polymerase - genetics; tobacco mosaic virus; Tobacco Mosaic Virus - genetics; Viral Proteins - genetics; Virology; VIRUS DE LA MOSAIQUE DU TABAC; VIRUS DEL MOSAICO DEL TABACO; Virus Replication - genetics; Virus; Enzyme; Tobacco mosaic virus; RNA polymerase RNA-dependent; Tobamovirus; Replication; Complementation; Mutation
• ISSN: 0042-6822; 1096-0341
• 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.