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植物的胁迫盐度:在可预见的情况下应对的新策略。

Stress salinity in plants: New strategies to cope with in the foreseeable scenario.

机构信息

Plant Molecular Biology Centre, Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile.

Instituto de Ciencias Biológicas. Universidad de Talca, Talca, Chile.

出版信息

Plant Physiol Biochem. 2024 Mar;208:108507. doi: 10.1016/j.plaphy.2024.108507. Epub 2024 Mar 5.

DOI:10.1016/j.plaphy.2024.108507
PMID:38467083
Abstract

The excess of salts in soils causes stress in most plants, except for some halophytes that can tolerate higher levels of salinity. The excess of Na generates an ionic imbalance, reducing the K content and altering cellular metabolism, thus impacting in plant growth and development. Additionally, salinity in soil induces water stress due to osmotic effects and increments the production of reactive oxygen species (ROS) that affect the cellular structure, damaging membranes and proteins, and altering the electrochemical potential of H, which directly affects nutrient absorption by membrane transporters. However, plants possess mechanisms to overcome the toxicity of the sodium ions, such as internalization into the vacuole or exclusion from the cell, synthesis of enzymes or protective compounds against ROS, and the synthesis of metabolites that help to regulate the osmotic potential of plants. Physiologic and molecular mechanisms of salinity tolerance in plants will be addressed in this review. Furthermore, a revision of strategies taken by researchers to confer salt stress tolerance on agriculturally important species are discussed. These strategies include conventional breeding and genetic engineering as transgenesis and genome editing by CRISPR/Cas9.

摘要

土壤中盐分过多会对大多数植物造成胁迫,除了一些能够耐受更高盐分水平的盐生植物。过量的钠离子会导致离子失衡,降低钾含量并改变细胞代谢,从而影响植物的生长和发育。此外,土壤中的盐分通过渗透作用引起水分胁迫,并增加活性氧(ROS)的产生,这会影响细胞结构,破坏膜和蛋白质,并改变 H 的电化学势,这直接影响膜转运体对养分的吸收。然而,植物具有克服钠离子毒性的机制,例如将钠离子内化到液泡中或从细胞中排除、合成对抗 ROS 的酶或保护化合物,以及合成有助于调节植物渗透势的代谢物。本文将讨论植物耐盐性的生理和分子机制。此外,还讨论了研究人员为赋予农业重要物种耐盐性而采取的策略。这些策略包括常规育种和遗传工程,如转基因和 CRISPR/Cas9 基因组编辑。

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