Specific Inhibition of Tobacco Mosaic Virus Protein and Single-Stranded RNA Synthesis by Arabinofuranosyladenine

Abstract

9-β-D-Arabinofuranosyladenine (ara A) was shown to inhibit a specific step of tobacco mosaic virus (TMV) multiplication. The time course of the ara A-sensitive function occurred ‘late’ coinciding with the period of viral RNA and protein synthesis. When treatment began after viral RNA synthesis was established, 1.0 mMara A inhibited viral single-stranded RNA and viral protein synthesis, but not viral double-stranded RNA synthesis. Viral double-stranded RNA synthesis was inhibited totally only when treatment with ara A began within the first 4 h (before any RNA synthesis was detected), and the degree of inhibition decreased rapidly when treatments began at later times. In contrast, single-stranded TMV RNA synthesis and viral protein synthesis were inhibited throughout the infection. The mode of action of ara A against TMV involves selective inhibition of a function required for single-stranded RNA synthesis and viral protein synthesis without detectable inhibition of RNA or protein synthesis of the host or ongoing viral double-stranded RNA synthesis.

Regulation of Tobamovirus Gene Expression

“…Ribovirin and low concentrations of guanidine inhibit with the same kinetics and might inhibit the same process (Dawson, 1975;Dawson and Lozoya-Saldana, 1984). Cycloheximide and arabinofuranosyladenine inhibit a later step that coincides with protein and RNA syntheses (Dawson and Schiegel, 1976a;Dawson and Lozoya-Saldana, 1986). When added to an infection in which virus replication is at the maximal rate, arabinofaranosyladenine inhibits the syntheses of single-stranded, but not double-stranded, RNA and viral proteins.…”

“…The second set of mutants was capable of synthesizing double-stranded, but not single-stranded, RNA; perhaps these mutants were defective, at the nonpermissive temperature, in a function that regulates plussense-minus-sense RNA ratios or is required to initiate plus-sense strands at the 3' terminus of minus-sense strands. Arabinofuranosyla-denine, when added to an ongoing infection, inhibits similarly (Dawson and Lozoya-Saldana, 1986).…”