An Ethylene-Induced Regulatory Module Delays Flower Senescence by Regulating Cytokinin Content.
Wu Lin,Ma Nan,Jia Yangchao,Zhang Yi,Feng Ming,Jiang Cai-Zhong,Ma Chao,Gao Junping
In many plant species, including rose (Rosa hybrida), flower senescence is promoted by the gaseous hormone ethylene and inhibited by the cytokinin (CTK) class of hormones. However, the molecular mechanisms underlying these antagonistic effects are not well understood. 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 reverse transcription PCR analysis showed that 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-Leu 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.
Transcription factor CDF4 promotes leaf senescence and floral organ abscission by regulating abscisic acid and reactive oxygen species pathways in Arabidopsis.
Xu Peipei,Chen Haiying,Cai Weiming
Leaf senescence is a highly complex developmental process that is tightly controlled by multiple layers of regulation. Abscisic acid (ABA) and reactive oxygen species (ROS) are two well-known factors that promote leaf senescence. We show here that the transcription factor CDF4 positively regulates leaf senescence. Constitutive and inducible overexpression of CDF4 accelerates leaf senescence, while knockdown of CDF4 delays it. CDF4 increases endogenous ABA levels by upregulating the transcription of the ABA biosynthesis genes 9-cis-epoxycarotenoid dioxygenase 2, 3 (NCED2, 3) and suppresses H O scavenging by repressing expression of the catalase2 (CAT2) gene. NCED2, 3 knockout and CAT2 overexpression partially rescue premature leaf senescence caused by CDF4 overexpression. We also show that CDF4 promotes floral organ abscission by activating the polygalacturonase PGAZAT gene. Based on these results, we propose that the levels of CDF4, ABA, and ROS undergo a gradual increase driven by their interlinking positive feedback loops during the leaf senescence and floral organ abscission processes.
Petal senescence: a hormone view.
Ma Nan,Ma Chao,Liu Yang,Shahid Muhammad Owais,Wang Chengpeng,Gao Junping
Journal of experimental botany
Flowers are highly complex organs that have evolved to enhance the reproductive success of angiosperms. As a key component of flowers, petals play a vital role in attracting pollinators and ensuring successful pollination. Having fulfilled this function, petals senesce through a process that involves many physiological and biochemical changes that also occur during leaf senescence. However, petal senescence is distinct, due to the abundance of secondary metabolites in petals and the fact that petal senescence is irreversible. Various phytohormones are involved in regulating petal senescence, and are thought to act both synergistically and antagonistically. In this regard, there appears to be developmental point during which such regulatory signals are sensed and senescence is initiated. Here, we review current understanding of petal senescence, and discuss associated regulatory mechanisms involving hormone interactions and epigenetic regulation.