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Global transcriptome analyses reveal that infection with chrysanthemum stunt viroid (CSVd) affects gene expression profile of chrysanthemum plants, but the genes involved in plant hormone metabolism and signaling may not be silencing target of CSVd-siRNAs

Takino, Hiroki, Kitajima, Sakihito, Hirano, Saki, Oka, Mariko, Matsuura, Takakazu, Ikeda, Yoko, Kojima, Mikiko, Takebayashi, Yumiko, Sakakibara, Hitoshi, Mino, Masanobu
Plant gene 2019 v.18 pp. 100181
Chrysanthemum, Chrysanthemum stunt viroid, abscisic acid, biosynthesis, cell walls, cytokinins, gene expression, gene silencing, genes, genomics, gibberellic acid, growth promotion, hormone metabolism, host plants, indole acetic acid, messenger RNA, nucleotide sequences, nucleotides, pathogenicity, plant diseases and disorders, plant growth, plant viruses
Chrysanthemum stunt viroid (CSVd) is a pathogen that induces stunted plant growth as a typical disease symptom in infected chrysanthemum plants. Because of its simple RNA genomic structure, the mechanism of how CSVd provokes pathogenicity in host plants remains elusive. Since small RNAs generated from CSVd genomic RNA accumulated in infected plants (Tsuro et al., 2013), it has been suggested that forced gene silencing against intrinsic genes by CSVd-small interfering (si)RNAs is involved in its pathogenicity. In this study, we revealed that CSVd infection induced global fluctuation of gene expression in plants. Hypothetical CSVd-siRNAs (22 nucleotides long) from (+) and (−) strands of the CSVd RNA genome were surveyed to examine if they could target the down-regulated gene sequences. Six genes were identified as target candidates, but the causal link between their functions and disease symptoms was remained unclear. In contrast, the expression levels of genes involved in the biosynthesis of gibberellic acid (GA) and cytokinin (CK), indole-3-acetic acid (IAA) transport and cell wall growth in infected plants were down-regulated, but mRNAs of those genes were not found as possible target sequences of CSVd-siRNAs. On the other hand, endogenous levels of GA, CK, IAA, and abscisic acid and the rate of IAA movement in the stem were not different between healthy and infected plants. Growth promotion of infected plants by GA treatment was poorer than that of healthy plants, suggesting that CSVd infection suppressed the GA-signaling pathway. This was further supported by the findings of a reduced response of GA-regulated genes to GA treatment and up-regulation of the DELLA-protein gene, a negative regulator of GA-signaling, in infected plants. Thus, the down-regulation of GA responsiveness and inhibition of cell wall expansion are major causes of the stunted growth of CSVd-infected chrysanthemum plants.