In roses (Rosa sp.), peduncle morphology is an important ornamental feature. The common physiological abnormality known as the bent peduncle phenomenon (BPP) seriously decreases the quality of rose flowers and thus the commercial value. Because the molecular mechanisms underlying this condition are poorly understood, we analysed the transcriptional profiles and cellular structures of bent rose peduncles. Numerous differentially expressed genes involved in the auxin, cytokinin, and gibberellin signaling pathways were shown to be associated with bent peduncle. Paraffin sections showed that the cell number on the upper sides of bent peduncles was increased, while the cells on the lower sides were larger than those in normal peduncles. We also investigated the large, deformed sepals that usually accompany BPP and found increased expression level of some auxin-responsive genes and decreased expression level of genes that are involved in cytokinin and gibberellin synthesis in these sepals. Furthermore, removal of the deformed sepals partially relieved BPP. In summary, our findings suggest that auxin, cytokinin, and gibberellin all influence the development of BPP by regulating cell division and expansion. To effectively reduce BPP in roses, more efforts need to be devoted to the molecular regulation of gibberellins and cytokinins in addition to that of auxin.
Rose plants are one of the most important horticultural crops, whose commercial value mainly depends on long-distance transportation, and wounding and ethylene are the main factors leading to their quality decline and accelerated senescence in the process. However, underlying molecular mechanisms of crosstalk between wounding and ethylene in the regulation of flower senescence remain poorly understood. In relation to this, transcriptome analysis was performed on rose flowers subjected to various treatments, including control, wounding, ethylene, and wounding- and ethylene- (EW) dual treatment. A large number of differentially expressed genes (DEGs) were identified, ranging from 2,442 between the ethylene- and control-treated groups to 4,055 between the EW- and control-treated groups. Using weighted gene co-expression network analysis (WGCNA), we identified a hub gene RhWRKY33 (rchiobhmchr5g0071811), accumulated in the nucleus, where it may function as a transcription factor. Moreover, quantitative reverse transcription PCR (RT-qPCR) results showed that the expression of RhWRKY33 was higher in the wounding-, ethylene, and EW-treated petals than in the control-treated petals. We also functionally characterized the RhWRKY33 gene through virus-induced gene silencing (VIGS). The silencing of RhWRKY33 significantly delayed the senescence process in the different treatments (control, wounding, ethylene, and EW). Meanwhile, we found that the effect of RhWRKY33-silenced petals under ethylene and EW dual-treatment were stronger than those under wounding treatment in delaying the petal senescence process, implying that RhWRKY33 is closely involved with ethylene and wounding mediated petal senescence. Overall, the results indicate that RhWRKY33 positively regulates the onset of floral senescence mediated by both ethylene and wounding signaling, but relies heavily on ethylene signaling.
The size of lateral organs is determined by well-coordinated cell proliferation and cell expansion. The transition from cell proliferation to expansion remains a largely unknown question in plant biology. Here, we report that miR159, an evolutionarily conserved microRNA, plays a crucial role in the transition from cell proliferation to expansion in rose (Rosa hybrida) petals through governing rapid cytokinin catabolism. We uncovered that Cytokinin Oxidase/Dehydrogenase 6 (CKX6) is an authentic target of miR159 in petals. Knocking down miR159 levels resulted in the accumulation of CKX6 transcripts and precocious cytokinin clearance, consequently leading to an earlier transition to cell expansion and smaller petals. Conversely, knockdown of CKX6 caused excess cytokinin and delayed cell expansion, mimicking the effects of exogenous cytokinin application. MYB73, a R2R3-type MYB transcription repressor, recruited a co-repressor (TOPLESS) and a histone deacetylase (HDA19) to form a suppression complex, which governed the expression of MIR159 by modulating H3K9 acetylation levels at the MIR159 promoter. This work thus provides insights for ensuring correct timing of cell expansion and organ size via control of cytokinin catabolism.
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