The plant hormones cytokinin (CK) and abscisic acid (ABA) play critical and often opposite roles during plant growth, development, and responses to abiotic and biotic stresses. Rose (Rosa sp.) is an economically important ornamental crop sold as cut flowers. Rose petals are extremely susceptible to gray mold disease caused by the necrotrophic fungal pathogen Botrytis cinerea. The infection of rose petals by B. cinerea leads to tissue collapse and rot, causing severe economic losses. In this study, we showed that CK and ABA play opposite roles in the susceptibility of rose to B. cinerea. Treatment with CK enhanced the disease protection of rose petals to B. cinerea, while ABA promoted disease progression. We further demonstrated that rose flowers activate CK-mediated disease protection via a B. cinerea-induced rose transcriptional repressor, Rosa hybrida (Rh)WRKY13, which is an ortholog of Arabidopsis (Arabidopsis thaliana), AtWRKY40. RhWRKY13 binds to promoter regions of the CK degradation gene CKX3 (RhCKX3) and the ABA-response gene ABA insensitive4 (RhABI4), leading to simultaneous inhibition of their expression in rose petals. The increased CK content and reduced ABA responses result in enhanced protection from B. cinerea. Collectively, these data reveal opposite roles for CK and ABA in the susceptibility of rose petals against B. cinerea infection, which is mediated by B. cinerea-induced RhWRKY13 expression.

The petals of ornamental plants such as roses (Rosa spp.) are the most economically important organs. This delicate, short-lived plant tissue is highly susceptible to pathogens, in large part because the walls of petal cells are typically thinner and more flexible compared with leaf cells, allowing the petals to fold and bend without breaking. The cell wall is a dynamic structure that rapidly alters its composition in response to pathogen infection, thereby reinforcing its stability and boosting plant resistance against diseases. However, little is known about how dynamic changes in the cell wall contribute to resistance to Botrytis cinerea in rose petals. Here, we show that the B. cinerea-induced transcription factor RhbZIP17 is required for the defense response of rose petals. RhbZIP17 is associated with phenylpropanoid biosynthesis and binds to the promoter of the lignin biosynthesis gene RhCAD1, activating its expression. Lignin content showed a significant increase under gray mold infection compared with the control. RhCAD1 functions in the metabolic regulation of lignin production and, consequently, disease resistance, as revealed by transient silencing and overexpression in rose petals. The WRKY transcription factor RhWRKY30 is also required to activate RhCAD1 expression and enhance resistance against B. cinerea. We propose that RhbZIP17 and RhWRKY30 increase lignin biosynthesis, improve the resistance of rose petals to B. cinerea, and regulate RhCAD1 expression.

Gray mold caused by the necrotrophic fungal pathogen Botrytis cinerea is one of the most destructive diseases in rose (Rosa spp.). Rose infection by B. cinerea leads to severe economic losses due to necrosis, tissue collapse, and rot. In rose, cytokinins (CK) positively regulate a defense response to B. cinerea, but little is known about the underlying molecular mechanisms. Here, we characterized two ethylene/jasmonic acid-regulated transcription factors, RhEFR005 and RhCCCH12, that bind to the promoter region of PATHOGENESIS-RELATED 10.1 (RhPR10.1) and promote its transcription, leading to decreased susceptibility to B. cinerea. RhEFR005/RhCCCH12-RhPR10.1 module induced cytokinin content in rose, and the susceptibility of RhEFR005-, RhCCCH12- and RhPR10.1-silenced rose petals can be rescued by exogenous CK. In summary, our results reveal that RhERF005/RhCCCH12-RhPR10.1 module regulates the CK-induced defense response of rose to B. cinerea.

Calcium-dependent protein kinases (CDPKs) function as essential sensors and transducers of intracellular calcium signals, playing crucial regulatory roles in various physiological processes. Nevertheless, studies on CDPK genes in Paeonia ostii remain limited. In this study, 16 PoCDPK genes containing a complete Pkinase domain and four EF-hand domains, distributed across five chromosomes, were identified in P. ostii. Phylogenetic analysis classified these genes into four distinct groups (I–IV). Promoter cis-element analysis suggested a potential involvement of PoCDPK genes in plant growth and development, phytohormone signaling, light, circadian, and stress responses. Transcription levels of PoCDPKs were highest at the early stage of root primordium formation (Gmfq) among the four stages examined. Expression analysis of the 14 PoCDPK genes detected in the transcriptome revealed that nine PoCDPKs were highly expressed in flowers, two in stems, PoCDPK10 in leaves, PoCDPK13 in roots, and PoCDPK1 in roots, stems, and leaves. Moreover, PoCDPK3, PoCDPK12, and PoCDPK13 from Group I, as well as PoCDPK2 and PoCDPK8 from Group III, were highly expressed at 5 d of rooting induction, suggesting their potential involvement in adventitious rooting. These findings provide a comprehensive reference for the potential functions of the CDPK family in the adventitious rooting of tree peony.