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<jats:title>Abstract</jats:title><jats:sec> <jats:title>Main conclusion</jats:title> <jats:p>Silencing of an ascorbate oxidase (<jats:italic>AO</jats:italic>) gene in <jats:italic>N. benthamiana</jats:italic> enhanced disease severity from cucumber mosaic virus (CMV), showing higher accumulation and expansion of the spreading area of CMV.</jats:p> </jats:sec><jats:sec> <jats:title>Abstract</jats:title> <jats:p>A <jats:italic>Nicotiana benthamiana</jats:italic> ascorbate oxidase (<jats:italic>NbAO</jats:italic>) gene was found to be induced upon cucumber mosaic virus (CMV) infection. Virus-induced gene silencing (VIGS) was employed to elucidate the function of AO in <jats:italic>N. benthamiana</jats:italic>. The tobacco rattle virus (TRV)-mediated VIGS resulted in an efficient silencing of the <jats:italic>NbAO</jats:italic> gene, i.e., 97.5% and 78.8% in relative quantification as compared to the control groups (TRV::eGFP- and the mock-inoculated plants), respectively. In addition, AO enzymatic activity decreased in the TRV::NtAO-silenced plants as compared to control. TRV::NtAO-mediated <jats:italic>NbAO</jats:italic> silencing induced a greater reduction in plant height by 15.2% upon CMV infection. CMV titer at 3 dpi was increased in the systemic leaves of <jats:italic>NbAO</jats:italic>-silenced plants (a 35-fold change difference as compared to the TRV::eGFP-treated group). Interestingly, CMV and TRV titers vary in different parts of systemically infected <jats:italic>N. benthamiana</jats:italic> leaves. In TRV::eGFP-treated plants, CMV accumulated only at the top half of the leaf, whereas the bottom half of the leaf was “occupied” by TRV. In contrast, in the <jats:italic>NbAO</jats:italic>-silenced plants, CMV accumulated in both the top and the bottom half of the leaf, suggesting that the silencing of the <jats:italic>NbAO</jats:italic> gene resulted in the expansion of the spreading area of CMV. Our data suggest that the <jats:italic>AO</jats:italic> gene might function as a resistant factor against CMV infection in <jats:italic>N. benthamiana</jats:italic>.</jats:p> </jats:sec>

<jats:title>Abstract</jats:title><jats:sec> <jats:title>Main conclusion</jats:title> <jats:p><jats:italic>OsNAC103</jats:italic> negatively regulates rice plant height by influencing the cell cycle and crosstalk of phytohormones.</jats:p> </jats:sec><jats:sec> <jats:title>Abstract</jats:title> <jats:p>Plant height is an important characteristic of rice farming and is directly related to agricultural yield. Although there has been great progress in research on plant growth regulation, numerous genes remain to be elucidated. NAC transcription factors are widespread in plants and have a vital function in plant growth. Here, we observed that the overexpression of <jats:italic>OsNAC103</jats:italic> resulted in a dwarf phenotype, whereas RNA interference (RNAi) plants and <jats:italic>osnac103</jats:italic> mutants showed no significant difference. Further investigation revealed that the cell length did not change, indicating that the dwarfing of plants was caused by a decrease in cell number due to cell cycle arrest. The content of the bioactive cytokinin N<jats:sup>6</jats:sup>-Δ<jats:sup>2</jats:sup>-isopentenyladenine (iP) decreased as a result of the cytokinin synthesis gene being downregulated and the enhanced degradation of cytokinin oxidase. <jats:italic>OsNAC103</jats:italic> overexpression also inhibited cell cycle progression and regulated the activity of the cell cyclin <jats:italic>OsCYCP2;1</jats:italic> to arrest the cell cycle. We propose that <jats:italic>OsNAC103</jats:italic> may further influence rice development and gibberellin–cytokinin crosstalk by regulating the <jats:italic>Oryza sativa homeobox 71</jats:italic> (<jats:italic>OSH71</jats:italic>). Collectively, these results offer novel perspectives on the role of <jats:italic>OsNAC103</jats:italic> in controlling plant architecture.</jats:p> </jats:sec>