了解植物的冷胁迫响应机制:综述。

IF 4.1 2区 生物学 Q1 PLANT SCIENCES
Frontiers in Plant Science Pub Date : 2024-11-06 eCollection Date: 2024-01-01 DOI:10.3389/fpls.2024.1443317
Zhenfeng Qian, Lilian He, Fusheng Li
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引用次数: 0

摘要

低温胁迫严重影响植物的生长、发育、产量和地理分布。然而,在长期的进化过程中,植物进化出了复杂的机制来抵抗低温胁迫。耐低温性状受多种途径调控,如 Ca2+ 信号级联、丝裂原活化蛋白激酶(MAPK)级联、CBF 表达诱导因子 1(ICE1)-C-重复结合因子(CBF)-冷调基因(COR)转录级联、活性氧(ROS)平衡调控和植物激素信号转导。然而,这些途径对冷胁迫的具体响应及其相互作用尚未完全清楚。本综述从冷信号感知与传导、ICE1-CBF-COR转录级联调控、ROS平衡调控和植物激素信号调控等四个方面总结了植物对冷胁迫的响应机制。研究还阐明了植物冷胁迫感知和Ca2+信号转导的机制,提出了转录因子(TFs)、翻译后修饰(PTMs)、光信号、昼夜节律时钟因子和互作蛋白在ICE1-CBF-COR转录级联中的重要作用。此外,我们还分析了 ROS 平衡和植物激素信号通路在植物冷胁迫响应中的重要性,并探讨了 ICE1-CBF-COR 级联、ROS 平衡和植物激素信号之间的交叉联系。这篇综述加深了我们对植物耐寒机制的理解,并为提高植物耐寒性的遗传策略提供了分子基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Understanding cold stress response mechanisms in plants: an overview.

Low-temperature stress significantly impacts plant growth, development, yield, and geographical distribution. However, during the long-term process of evolution, plants have evolved complicated mechanisms to resist low-temperature stress. The cold tolerance trait is regulated by multiple pathways, such as the Ca2+ signaling cascade, mitogen-activated protein kinase (MAPK) cascade, inducer of CBF expression 1 (ICE1)-C-repeat binding factor (CBF)-cold-reulated gene (COR) transcriptional cascade, reactive oxygen species (ROS) homeostasis regulation, and plant hormone signaling. However, the specific responses of these pathways to cold stress and their interactions are not fully understood. This review summarizes the response mechanisms of plants to cold stress from four aspects, including cold signal perception and transduction, ICE1-CBF-COR transcription cascade regulation, ROS homeostasis regulation and plant hormone signal regulation. It also elucidates the mechanism of cold stress perception and Ca2+ signal transduction in plants, and proposes the important roles of transcription factors (TFs), post-translational modifications (PTMs), light signals, circadian clock factors, and interaction proteins in the ICE1-CBF-COR transcription cascade. Additionally, we analyze the importance of ROS homeostasis and plant hormone signaling pathways in plant cold stress response, and explore the cross interconnections among the ICE1-CBF-COR cascade, ROS homeostasis, and plant hormone signaling. This comprehensive review enhances our understanding of the mechanism of plant cold tolerance and provides a molecular basis for genetic strategies to improve plant cold tolerance.

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来源期刊
Frontiers in Plant Science
Frontiers in Plant Science PLANT SCIENCES-
CiteScore
7.30
自引率
14.30%
发文量
4844
审稿时长
14 weeks
期刊介绍: In an ever changing world, plant science is of the utmost importance for securing the future well-being of humankind. Plants provide oxygen, food, feed, fibers, and building materials. In addition, they are a diverse source of industrial and pharmaceutical chemicals. Plants are centrally important to the health of ecosystems, and their understanding is critical for learning how to manage and maintain a sustainable biosphere. Plant science is extremely interdisciplinary, reaching from agricultural science to paleobotany, and molecular physiology to ecology. It uses the latest developments in computer science, optics, molecular biology and genomics to address challenges in model systems, agricultural crops, and ecosystems. Plant science research inquires into the form, function, development, diversity, reproduction, evolution and uses of both higher and lower plants and their interactions with other organisms throughout the biosphere. Frontiers in Plant Science welcomes outstanding contributions in any field of plant science from basic to applied research, from organismal to molecular studies, from single plant analysis to studies of populations and whole ecosystems, and from molecular to biophysical to computational approaches. Frontiers in Plant Science publishes articles on the most outstanding discoveries across a wide research spectrum of Plant Science. The mission of Frontiers in Plant Science is to bring all relevant Plant Science areas together on a single platform.
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