Summary: C ucumber 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 CMV s. 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 ( CPRG s) 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 CPRG s, which are closely associated with the induction of chlorosis.

In Arabidopsis, the IRE1A and IRE1B double mutant (ire1a/b) is unable to activate cytoplasmic splicing of bZIP60 mRNA and regulated IRE1-dependent decay under ER stress, whereas the mutant does not exhibit severe developmental defects under normal conditions. In this study, we focused on the Arabidopsis IRE1C gene, whose product lacks a sensor domain. We found that the ire1a/b/c triple mutant is lethal, and heterozygous IRE1C (ire1c/+) mutation in the ire1a/b mutants resulted in growth defects and reduction of the number of pollen grains. Genetic analysis revealed that IRE1C is required for male gametophyte development in the ire1a/b mutant background. Expression of a mutant form of IRE1B that lacks the luminal sensor domain (ΔLD) complemented a developmental defect in the male gametophyte in ire1a/b/c haplotype. In vivo, the ΔLD protein was activated by glycerol treatment that increases the composition of saturated lipid and was able to activate regulated IRE1-dependent decay but not bZIP60 splicing. These observations suggest that IRE1 contributes to plant development, especially male gametogenesis, using an alternative activation mechanism that bypasses the unfolded protein-sensing luminal domain.