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BpEIN3.1 通过抑制白桦中乙烯和脱落酸的合成来抑制叶片衰老。

BpEIN3.1 represses leaf senescence by inhibiting synthesis of ethylene and abscisic acid in Betula platyphylla.

机构信息

State Key Laboratory of Tree Genetics and Breeding, Northeast Forestry University, Harbin 150040, China.

Citrus Research and Education Center, University of Florida, Lake Alfred, FL 33850, United States.

出版信息

Plant Sci. 2022 Aug;321:111330. doi: 10.1016/j.plantsci.2022.111330. Epub 2022 May 25.

Abstract

Leaf senescence and abscission play crucial role in annual plant adapting to seasonal alteration and climate changes by shortening life cycle and development process in response to abiotic and/or biotic stressors underlying phytohormones and environmental signals. Ethylene and abscisic acid are the major phytohormones that promotes leaf senescence, involving various transcription factors, such as EIN3 (ethylene-insensitive 3) and EIL (ethylene-insensitive 3-like) gene family, controlling leaf senescence through metabolite biosynthesis and signal transduction pathways. However, the roles of EIN3 regulating leaf senescence responding to environmental changes in perennial plant, especially forestry tree, remain unclear. In this study, we found that BpEIN3.1 from a subordinated to EIL3 subclade, is a transcription repressor and regulated light-dependent premature leaf senescence in birch (Betula platyphylla). BpEIN3.1 might inhibits the transcription of BpATPS1 by binding to its promoter. Shading suppressed premature leaf senescence in birch ein3.1 mutant line. Ethylene and abscisic acid biosynthesis were also reduced. In addition, abscisic acid positively regulated the expression of BpEIN3.1. This was demonstrated by the hormone-response element analysis of BpEIN3.1 promoter and its gene expression after the hormone treatments. Moreover, our results showed that abscisic acid is also involved in maintaining homeostasis. The molecular mechanism of leaf senescence provides a possibility to increasing wood production by delaying of leaf senescence.

摘要

叶片衰老和脱落对于一年生植物适应季节性变化和气候变化至关重要,它们通过缩短生命周期和发育过程来应对潜在的生物和非生物胁迫,响应植物激素和环境信号。乙烯和脱落酸是促进叶片衰老的主要植物激素,涉及各种转录因子,如 EIN3(乙烯不敏感 3)和 EIL(乙烯不敏感 3 样)基因家族,通过代谢物生物合成和信号转导途径控制叶片衰老。然而,EIN3 在多年生植物(尤其是林业树木)中调节叶片衰老以响应环境变化的作用仍不清楚。在这项研究中,我们发现,从属 EIL3 亚家族的 BpEIN3.1 是一个转录抑制子,调控白桦(Betula platyphylla)中光依赖性的过早叶片衰老。BpEIN3.1 可能通过结合其启动子抑制 BpATPS1 的转录。遮荫抑制了白桦 ein3.1 突变体系中过早的叶片衰老。乙烯和脱落酸的生物合成也减少了。此外,脱落酸正向调节 BpEIN3.1 的表达。这可以通过对 BpEIN3.1 启动子的激素反应元件分析及其在激素处理后的基因表达来证明。此外,我们的结果表明,脱落酸也参与维持内稳态。叶片衰老的分子机制为通过延迟叶片衰老来增加木材产量提供了可能性。

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