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The leaf senescence-promoting transcription factor AtNAP activates its direct target gene CYTOKININ OXIDASE 3 to facilitate senescence processes by degrading cytokinins.促进叶片衰老的转录因子AtNAP激活其直接靶基因细胞分裂素氧化酶3,通过降解细胞分裂素来促进衰老过程。
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A positive feedback regulatory loop, SA-AtNAP-SAG202/SARD1-ICS1-SA, in SA biosynthesis involved in leaf senescence but not defense response.一个正反馈调节环SA-AtNAP-SAG202/SARD1-ICS1-SA参与叶片衰老过程中的水杨酸生物合成,但不参与防御反应。
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NAC 转录因子 TgNAP 促进郁金香花瓣衰老。

NAC transcription factor TgNAP promotes tulip petal senescence.

机构信息

Key Laboratory of Horticultural Plant Biology, Ministry of Education, College of Horticulture and Forestry Sciences, Huazhong Agricultural University, Wuhan 430070, PR China.

National R&D Centre for Citrus Preservation, Huazhong Agricultural University, Wuhan 430070, PR China.

出版信息

Plant Physiol. 2022 Oct 27;190(3):1960-1977. doi: 10.1093/plphys/kiac351.

DOI:10.1093/plphys/kiac351
PMID:35900170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9614467/
Abstract

Petal senescence is a crucial determinant for ornamental quality and economic value of floral crops. Salicylic acid (SA) and reactive oxygen species (ROS) are two prominent factors involved in plant senescence regulation. In this study, tulip TgNAP (NAC-like, activated by APETALA3/PISTILLATA) was characterized as positively regulating tulip petal senescence through dually regulating SA biosynthesis and ROS detoxification pathways. TgNAP was upregulated in senescing petals of tulip while exogenous SA and H2O2 treatments substantially promoted petal senescence in tulip. Silencing of TgNAP by VIGS assay delayed SA and H2O2-induced petal senescence in tulip, whereas overexpression of TgNAP promoted the senescence process in Arabidopsis (Arabidopsis thaliana) plants. Additionally, inhibition of SA biosynthesis prolonged the lifespan of TgNAP-silenced petal discs. Further evidence indicated that TgNAP activates the transcriptions of two key SA biosynthetic genes ISOCHORISMATE SYNTHASE 1 (TgICS1) and PHENYLALANINE AMMONIA-LYASE 1 (TgPAL1) through directly binding to their promoter regions. Meanwhile, TgNAP repressed ROS scavenging by directly inhibiting PEROXIDASE 12 (POD12) and POD17 expression. Taken together, these results indicate that TgNAP enhances SA biosynthesis and ROS accumulation to positively regulate petal senescence in tulip.

摘要

花瓣衰老对于花卉作物的观赏品质和经济价值是一个至关重要的决定因素。水杨酸(SA)和活性氧(ROS)是参与植物衰老调控的两个重要因素。在这项研究中,郁金香 TgNAP(NAC 样蛋白,由 APETALA3/PISTILLATA 激活)被鉴定为通过双重调节 SA 生物合成和 ROS 解毒途径来正向调控郁金香花瓣衰老。在郁金香衰老的花瓣中,TgNAP 上调,而外源 SA 和 H2O2 处理则显著促进了郁金香的花瓣衰老。VIGS 实验沉默 TgNAP 会延迟 SA 和 H2O2 诱导的郁金香花瓣衰老,而过表达 TgNAP 则会促进拟南芥(Arabidopsis thaliana)植物的衰老过程。此外,抑制 SA 生物合成会延长沉默 TgNAP 的花瓣圆盘的寿命。进一步的证据表明,TgNAP 通过直接结合其启动子区域,激活两个关键的 SA 生物合成基因异分支酸合酶 1(TgICS1)和苯丙氨酸氨解酶 1(TgPAL1)的转录。同时,TgNAP 通过直接抑制过氧化物酶 12(POD12)和 POD17 的表达来抑制 ROS 清除。综上所述,这些结果表明 TgNAP 通过增强 SA 生物合成和 ROS 积累来正向调控郁金香花瓣衰老。