Journal
ARCHIVES OF VIROLOGY
Volume 151, Issue 4, Pages 721-733Publisher
SPRINGER WIEN
DOI: 10.1007/s00705-005-0658-y
Keywords
-
Categories
Funding
- NIGMS NIH HHS [GM064465-01A2] Funding Source: Medline
Ask authors/readers for more resources
The replication competence of a series of brome mosaic virus (BMV) RNA1 variants with defined mutations in the 3 ' tRNA-like structure, previously characterized in vitro to be defective in minus-strand synthesis and several tRNA-associated functions, was analyzed in barley protoplasts. Inocula containing wild type RNAs2 and 3 and RNA1 bearing either Delta knob or 5 ' Psk mutation failed to replicate. Two additional RNA1 variants, each bearing either M4 or 5 ' AGA mutation, resulted in detectable accumulation of progeny but are inhibitory to overall viral replication when supplied in high concentrations. Another aminoacylation-defective mutation Delta 5 ' supported viral replication but did not interfere with viral replication even at higher concentrations. Coinoculation of replication-incompetent variants of RNAl with wt RNAs2 and 3 to Chenopodium hybridum plants resulted in the delayed development of local necrotic lesions characteristic of a wt infection. Sequence analysis of progeny RNA recovered from these lesions indicated that, in each case, a functional 3 ' noncoding sequence was restored due to homologous recombination with a corresponding sequence from wt RNA3. Taken together the results suggest that, unlike protein 2a which is required in catalytic amounts, the intrinsic involvement of protein 1a at various stages of virus infection cycle demands its sustained synthesis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available