Affiliation:
1. Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589
2. CREST, Japan Science and Technology Corporation, Kawaguchi, Saitama 322-0012, Japan
Abstract
ABSTRACT
The
cum1
and
cum2
mutations of
Arabidopsis thaliana
inhibit cucumber mosaic virus (CMV) multiplication. In
cum1
and
cum2
protoplasts, CMV RNA and the coat protein accumulated to wild-type levels, but the accumulation of the 3a protein of CMV, which is necessary for cell-to-cell movement of the virus, was strongly reduced compared with that in wild-type protoplasts. In
cum2
protoplasts, the accumulation of turnip crinkle virus (TCV)-related RNA and proteins was also reduced. Positional cloning demonstrated that
CUM1
and
CUM2
encode eukaryotic translation initiation factors 4E and 4G, respectively. Unlike most cellular mRNA, the CMV RNA lacks a poly(A) tail, whereas the TCV RNA lacks both a 5′-terminal cap and a poly(A) tail. In vivo translation analyses, using chimeric luciferase mRNA carrying the terminal structures and untranslated sequences of the CMV or TCV RNA, demonstrated that these viral untranslated sequences contain elements that regulate the expression of encoded proteins positively or negatively. The
cum1
and
cum2
mutations had different effects on the action of these elements, suggesting that the
cum1
and
cum2
mutations cause inefficient production of CMV 3a protein and that the
cum2
mutation affects the production of TCV-encoded proteins.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
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