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ARS Home » Pacific West Area » Davis, California » Crops Pathology and Genetics Research » Research » Publications at this Location » Publication #336381

Research Project: Improvement of Postharvest Performance of Ornamentals Using Molecular Genetic Approaches

Location: Crops Pathology and Genetics Research

Title: An ethylene-induced regulatory module delays rose flower senescence by regulating cytokinin content

Author
item Wu, Lin - China Agricultural University
item Ma, Nan - China Agricultural University
item Jia, Yangchao - China Agricultural University
item Zhang, Yi - China Agricultural University
item Feng, Ming - China Agricultural University
item Jiang, Cai-zhong
item Ma, Chao - China Agricultural University
item Gao, Junping - China Agricultural University

Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/20/2016
Publication Date: 1/3/2017
Citation: Wu, L., Ma, N., Jia, Y., Zhang, Y., Feng, M., Jiang, C., Ma, C., Gao, J. 2017. An ethylene-induced regulatory module delays rose flower senescence by regulating cytokinin content. Plant Physiology. 173(1):853-862. doi: 10.1104/pp.16.01064.

Interpretive Summary: The terminal phase of flower development is senescence, a highly regulated process that exhibits a hallmark of programmed cell death including many of the structural, biochemical, and molecular changes. The initiation of flower senescence can be triggered by external or internal cues. Phytohormones have been shown to play a pivotal role in triggering and modulating the progression of senescence, often through combinatorial interactions. Among these hormones, ethylene is considered a major regulator of flower senescence, and in ethylene-sensitive species, flower senescence is associated with a burst of ethylene production, and the coordinated expression of ethylene-responsive genes, including those with regulatory functions. Members of another class of hormones, cytokinins (CTKs), have been proposed to act as anti-senescence factors in flowers. In addition to the individual effects of ethylene and CTK on flower senescence, these two hormones have been reported to interact in senescence. However, despite such observations exemplifying the antagonistic effects of ethylene and CTKs on flower senescence, the underlying molecular mechanisms and the many details of the genes in the associated regulatory networks are still largely unknown. In this study of rose flower senescence, we identified a member of pathogenesis-related (PR) PR-10 family as being involved in the crosstalk between ethylene and CTK signaling. PR proteins, which function in a wide range of processes related to signal transduction and antimicrobial activity, have been classified into 17 families based on structural features, of these, the PR-10 protein family is a large group containing more than 100 members, which are typically small and localized in the cytosol. PR-10 proteins play multifunctional roles in defense mechanisms against abiotic and biotic stresses, and in developmental regulation via their RNase activity and/or interaction with ligands. In addition, CTKs can play a role in biological processes that are mediated by PR-10 proteins. It has been proposed that when PR-10 proteins act as RNases, they may degrade certain types of tRNAs containing a CTK moiety, thereby contributing to the regulation of endogenous CTK content. In support of this idea, over-expression of the pea (Pisum sativum) PR-10 gene, ABR17, in Brassica napus and A. thaliana enhanced abiotic stress tolerance through degradation of RNA to increase CTK levels. PR-10 proteins are also capable of binding CTKs; LIPR-10.2 from yellow lupine (Lupinus arboreus), has been shown to bind trans-zeatin, thereby acting as a reservoir of CTK molecules. However, the role of PR-10 proteins in modulating CTK content during flower senescence has not been characterized. Roses are one of the most important ornamental crops worldwide, and its commodity value largely depends on a long vase life of the flower. It is well-known that ethylene promotes rose flower senescence, while CTKs delay the process. In this study, we characterized the association between a pathogenesis related PR-10 family gene from rose (RhPR10.1) and the hormonal regulation of flower senescence. Quantitative RT-PCR analysis showed that the RhPR10.1 was expressed at high levels during senescence in different floral organs, including petal, sepal, receptacle, stamen, and pistil, and that expression was induced by ethylene treatment. Silencing of RhPR10.1 expression in rose plants by virus induced gene silencing accelerated flower senescence, which was accompanied by a higher ion leakage rate in the petals, as well as increased expression of the senescence marker gene, RhSAG12. CTK content and the expression of three CTK signaling pathway genes were reduced in RhPR10.1-silenced plants, and the accelerated rate of petal senescence that was apparent in the RhPR10.1-silenced plants was restored to normal levels by CTK treatment. Finally, RhHB6, a ho

Technical Abstract: In many plant species, including rose (Rosa hybrida), flower senescence is promoted by the gaseous hormone, ethylene, and inhibited by cytokinin (CTK) class of hormones. However, the molecular mechanisms underlying these antagonistic effects are not well understood. In this current study, we characterized the association between a pathogenesis related PR-10 family gene from rose (RhPR10.1) and the hormonal regulation of flower senescence. Quantitative RT-PCR analysis showed that the RhPR10.1 was expressed at high levels during senescence in different floral organs, including petal, sepal, receptacle, stamen, and pistil, and that expression was induced by ethylene treatment. Silencing of RhPR10.1 expression in rose plants by virus induced gene silencing accelerated flower senescence, which was accompanied by a higher ion leakage rate in the petals, as well as increased expression of the senescence marker gene, RhSAG12. CTK content and the expression of three CTK signaling pathway genes were reduced in RhPR10.1-silenced plants, and the accelerated rate of petal senescence that was apparent in the RhPR10.1-silenced plants was restored to normal levels by CTK treatment. Finally, RhHB6, a homeodomain-leucine zipper I transcription factor, was observed to bind to the RhPR10.1 promoter, and silencing of its expression also promoted flower senescence. Our results reveal an ethylene-induced RhHB6-RhPR10.1 regulatory module that functions as a brake of ethylene-promoted senescence through increasing the CTK content.