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Cucumber mosaic virus (CMV) causes mosaic disease in inoculated tobacco plants. Coat protein (CP) is one of the major virulence determinants of CMV, and an amino acid substitution at residue 129 in CP alters the severity of chlorosis, such as pale green chlorosis and white chlorosis, in symptomatic tissues of mosaic leaves of infected tobacco. In this study, we compared the transcriptomes of chlorotic tissues infected with the wild-type pepo strain of CMV and two strains carrying CP mutants with diverse chlorosis severity. Differential gene expression analysis showed that CMV inoculation appeared to have similar effects on the transcriptional expression profiles of the symptomatic chlorotic tissues, and only the magnitude of expression differed among the different CMVs. Gene ontology analysis with biological process and cellular component terms revealed that many nuclear genes related to abiotic stress responses, including responses to cadmium, heat, cold and salt, were up-regulated, whereas chloroplast- and photosynthesis-related genes (CPRGs) were down-regulated, in the chlorotic tissues. Interestingly, the level of CPRG down-regulation was correlated with the severity of chlorosis. These results indicate that CP mutation governs the repression level and mRNA accumulation of CPRGs, which are closely associated with the induction of chlorosis.

SUMMARY Taxonomic relationships:Cucumber mosaic virus (CMV) is the type species of the genus Cucumovirus in the family Bromoviridae, which also encompasses the Peanut stunt virus (PSV) and the Tomato aspermy virus (TAV). Nucleotide sequence similarity among these three cucumoviruses is 60%–65%. CMV strains are divided into three subgroups, IA, IB and II, based on the sequence of the 5′ untranslated region of the genomic RNA 3. Overall nucleotide sequence similarity among CMV strains is approximately 70%–98%. Geographical distribution, host range and symptomatology: CMV is distributed worldwide, primarily in temperate to tropical climate zones. CMV infects more than 1200 species of 100 plant families, including monocot and dicot plants. Symptoms caused by CMV infection vary with the host species and/or CMV strain, and include mosaic, stunt, chlorosis, dwarfing, leaf malformation and systemic necrosis. CMV disease is spread primarily by aphid transmission in a nonpersistent manner. Physical properties: In tobacco sap, the thermal inactivation point of the viral infectivity is approximately 70 °C (10 min), the dilution end-point is approximately 10−4 and viral infectivity is lost after a few days of exposure to 20 °C. Viral infectivity can be retained in freeze-dried tissues and in the form of virions purified using 5 mm sodium borate, 0.5 mm ethylenediaminetetraacetic acid and 50% glycerol (pH 9.0) at −20 °C. CMV particles are isometric, approximately 28–30 nm in diameter and are composed of 180 capsid subunits arranged in pentamer–hexamer clusters with T= 3 symmetry. The sedimentation coefficient (s20,w) is c. 98 S and the particle weight is (5.8–6.7) × 106 Da. The virions contain 18% RNA. The RNA–protein interactions that stabilize the CMV virions are readily disrupted by sodium dodecylsulphate or neutral chloride salts. Genomic properties: The genomic RNAs are single-stranded messenger sense RNAs with 5′ cap and 3′ tRNA-like structures containing at least five open reading frames. The viral RNA consists of three genomic RNAs, RNA 1 (c. 3.3 kb), RNA 2 (c. 3.0 kb) and RNA 3 (c. 2.2 kb), and two subgenomic RNAs, RNA 4 (c. 1.0 kb) and RNA 4A (c. 0.7 kb). The 3′ untranslated regions are conserved across all viral RNAs. CMV is often accompanied by satellite, noncoding, small, linear RNA that is nonhomologous to the helper CMV. Useful websites:http://www.dpvweb.net/dpv/showdpv.php?dpvno=400 (general information); http://www.rcsb.org/pdb/explore/explore.do?pdbId=1f15 (structure).