A petunia transcription factor, PhOBF1, regulates flower senescence by modulating gibberellin biosynthesis.

IF 7.6 Q1 GENETICS & HEREDITY 园艺研究(英文) Pub Date : 2023-02-16 eCollection Date: 2023-04-01 DOI:10.1093/hr/uhad022
Xiaotong Ji, Ziwei Xin, Yanping Yuan, Meiling Wang, Xinyi Lu, Jiaqi Li, Yanlong Zhang, Lixin Niu, Cai-Zhong Jiang, Daoyang Sun
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Abstract

Flower senescence is commonly enhanced by the endogenous hormone ethylene and suppressed by the gibberellins (GAs) in plants. However, the detailed mechanisms for the antagonism of these hormones during flower senescence remain elusive. In this study, we characterized one up-regulated gene PhOBF1, belonging to the basic leucine zipper transcription factor family, in senescing petals of petunia (Petunia hybrida). Exogenous treatments with ethylene and GA3 provoked a dramatic increase in PhOBF1 transcripts. Compared with wild-type plants, PhOBF1-RNAi transgenic petunia plants exhibited shortened flower longevity, while overexpression of PhOBF1 resulted in delayed flower senescence. Transcript abundances of two senescence-related genes PhSAG12 and PhSAG29 were higher in PhOBF1-silenced plants but lower in PhOBF1-overexpressing plants. Silencing and overexpression of PhOBF1 affected expression levels of a few genes involved in the GA biosynthesis and signaling pathways, as well as accumulation levels of bioactive GAs GA1 and GA3. Application of GA3 restored the accelerated petal senescence to normal levels in PhOBF1-RNAi transgenic petunia lines, and reduced ethylene release and transcription of three ethylene biosynthetic genes PhACO1, PhACS1, and PhACS2. Moreover, PhOBF1 was observed to specifically bind to the PhGA20ox3 promoter containing a G-box motif. Transient silencing of PhGA20ox3 in petunia plants through tobacco rattle virus-based virus-induced gene silencing method led to accelerated corolla senescence. Our results suggest that PhOBF1 functions as a negative regulator of ethylene-mediated flower senescence by modulating the GA production.

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矮牵牛转录因子PhOBF1通过调节赤霉素的生物合成来调节花朵衰老。
植物中的花衰老通常由内源激素乙烯促进,而赤霉素(GA)抑制。然而,这些激素在花朵衰老过程中拮抗作用的详细机制仍然难以捉摸。在本研究中,我们在矮牵牛(petunia hybrida)衰老花瓣中鉴定了一个上调的基因PhOBF1,属于碱性亮氨酸拉链转录因子家族。用乙烯和GA3的外源处理引起PhOBF1转录物的显著增加。与野生型植物相比,PhOBF1-RNAi转基因矮牵牛植物的花寿命缩短,而PhOBF1的过表达导致花衰老延迟。两个衰老相关基因PhSAG12和PhSAG29的转录丰度在PhOBF1沉默的植物中较高,但在PhOBF1-过表达的植物中较低。PhOBF1的沉默和过表达影响了参与GA生物合成和信号通路的少数基因的表达水平,以及生物活性GA GA1和GA3的积累水平。GA3的应用使PhOBF1-RNAi转基因矮牵牛系的加速花瓣衰老恢复到正常水平,并减少了三个乙烯生物合成基因PhACO1、PhACS1和PhACS2的乙烯释放和转录。此外,观察到PhOBF1与含有G-box基序的PhGA20ox3启动子特异性结合。通过基于烟草拨浪鼓病毒的病毒诱导的基因沉默方法在矮牵牛植株中短暂沉默PhGA20ox3,导致花冠衰老加速。我们的研究结果表明,PhOBF1通过调节GA的产生,对乙烯介导的花朵衰老起到负调控作用。
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