RhMYB108, an R2R3-MYB transcription factor, is involved in ethylene- and JA-induced petal senescence in rose plants

Shuai Zhang,Nan Ma,Daxing Zeng,Yonghong Li,Qingcui Zhao,Jiehua Xu,Fenglan Wang,Hougao Zhou

doi:10.1038/s41438-019-0221-8

Abstract

Rose (Rosa hybrida) plants are major ornamental species worldwide, and their commercial value greatly depends on their open flowers, as both the quality of fully open petals and long vase life are important. Petal senescence can be started and accelerated by various hormone signals, and ethylene is considered an accelerator of petal senescence in rose. To date, however, the underlying mechanism of signaling crosstalk between ethylene and other hormones such as JA in petal senescence remains largely unknown. Here, we isolated RhMYB108, an R2R3-MYB transcription factor, which is highly expressed in senescing petals as well as in petals treated with exogenous ethylene and JA. Applications of exogenous ethylene and JA markedly accelerated petal senescence, while the process was delayed in response to applications of 1-MCP, an ethylene action inhibitor. In addition, silencing of RhMYB108 alter the expression of SAGs such as RhNAC029, RhNAC053, RhNAC092, RhSAG12, and RhSAG113, and finally block ethylene- and JA-induced petal senescence. Furthermore, RhMYB108 was identified to target the promoters of RhNAC053, RhNAC092, and RhSAG113. Our results reveal a model in which RhMYB108 functions as a receptor of ethylene and JA signals to modulate the onset of petal senescence by targeting and enhancing senescence-associated gene expression.

Highlights

Petals are a key component of flowers, and by attracting pollinators, they play a vital role in ensuring successful pollination[1]
Ethylene and jasmonic acid (JA) accelerate the senescence of rose petals The function of ethylene and JA in the acceleration of leaf senescence has been widely reported[21,25], but the interaction and crosstalk between these hormones during flower senescence has not been studied in detail
The transcript levels of senescenceassociated genes (SAGs) RhSAG12, a molecular marker of rose petal senescence progression, were significantly higher in the hormone-treated petal discs than in the control discs (Fig. 1d). Compared with those treated with ethylene or JA, the petal discs treated with 1-MCP, a powerful antagonist of ethylene action, presented a slight color loss (Fig. 1a), and this result was supported by the experimental data concerning the color fading rate (Fig. 1b), ion leakage rate (Fig. 1c), and RhSAG12 expression (Fig. 1d)

Summary

Introduction

Petals are a key component of flowers, and by attracting pollinators, they play a vital role in ensuring successful pollination[1]. Petal senescence is a natural and irreversible process that occurs at the terminal stage of flower development and is tightly controlled by environmental and developmental signals. Many excellent studies have reported that multiple vital activities are involved in petal senescence, such as programmed cell death (PCD)[4,5,6], sugar metabolism[7], hormone regulation[8,9], and the regulatory activity of associated gene networks[10,11,12]. The onset of petal senescence is initiated by external and internal cues, and phytohormones have been revealed to act as essential signals in initiating and modulating the senescence process. The role of jasmonic acid (JA) and auxin in petal senescence is still unknown[10]

Methods

Results

Conclusion