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氯离子通道从高尔基体向质膜的易位有助于植物适应盐胁迫。

The translocation of a chloride channel from the Golgi to the plasma membrane helps plants adapt to salt stress.

机构信息

Department of Biological Sciences and Research Centre on Sustainable Urban Farming, National University of Singapore, 14 Science Drive 4, Singapore, 117543, Singapore.

NUS Environmental Research Institute, National University of Singapore, #02-01, T-Lab Building, 5A Engineering Drive 1, Singapore, 117411, Singapore.

出版信息

Nat Commun. 2024 May 10;15(1):3978. doi: 10.1038/s41467-024-48234-z.

DOI:10.1038/s41467-024-48234-z
PMID:38729926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11087495/
Abstract

A key mechanism employed by plants to adapt to salinity stress involves maintaining ion homeostasis via the actions of ion transporters. While the function of cation transporters in maintaining ion homeostasis in plants has been extensively studied, little is known about the roles of their anion counterparts in this process. Here, we describe a mechanism of salt adaptation in plants. We characterized the chloride channel (CLC) gene AtCLCf, whose expression is regulated by WRKY transcription factor under salt stress in Arabidopsis thaliana. Loss-of-function atclcf seedlings show increased sensitivity to salt, whereas AtCLCf overexpression confers enhanced resistance to salt stress. Salt stress induces the translocation of GFP-AtCLCf fusion protein to the plasma membrane (PM). Blocking AtCLCf translocation using the exocytosis inhibitor brefeldin-A or mutating the small GTPase gene AtRABA1b/BEX5 (RAS GENES FROM RAT BRAINA1b homolog) increases salt sensitivity in plants. Electrophysiology and liposome-based assays confirm the Cl/H antiport function of AtCLCf. Therefore, we have uncovered a mechanism of plant adaptation to salt stress involving the NaCl-induced translocation of AtCLCf to the PM, thus facilitating Cl removal at the roots, and increasing the plant's salinity tolerance.

摘要

植物适应盐胁迫的一个关键机制涉及通过离子转运蛋白的作用维持离子稳态。虽然阳离子转运蛋白在植物维持离子稳态中的功能已得到广泛研究,但阴离子转运蛋白在这一过程中的作用知之甚少。在这里,我们描述了植物耐盐的一种机制。我们对氯离子通道(CLC)基因 AtCLCf 进行了表征,该基因在拟南芥中受 WRKY 转录因子调控,在盐胁迫下表达。atclcf 功能丧失型幼苗对盐更敏感,而过表达 AtCLCf 则增强了对盐胁迫的抗性。盐胁迫诱导 GFP-AtCLCf 融合蛋白向质膜(PM)的易位。使用胞吐抑制剂布雷菲德菌素 A 或突变小 GTP 酶基因 AtRABA1b/BEX5(源自大鼠脑 A1b 的 RAS 基因同源物)阻断 AtCLCf 的易位会增加植物对盐的敏感性。电生理学和脂质体测定证实了 AtCLCf 的 Cl/H 反向转运功能。因此,我们揭示了一种植物适应盐胁迫的机制,涉及 NaCl 诱导 AtCLCf 向 PM 的易位,从而促进根部 Cl 的去除,并提高植物的耐盐性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/82378348a65e/41467_2024_48234_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/f280266abc13/41467_2024_48234_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/3fa89bf463bb/41467_2024_48234_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/fedd21a5c073/41467_2024_48234_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/7e2e8456a67a/41467_2024_48234_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/999d9908fd9b/41467_2024_48234_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/b4fe61f96ab2/41467_2024_48234_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/82378348a65e/41467_2024_48234_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/f280266abc13/41467_2024_48234_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/3fa89bf463bb/41467_2024_48234_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/fedd21a5c073/41467_2024_48234_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/7e2e8456a67a/41467_2024_48234_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/999d9908fd9b/41467_2024_48234_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/b4fe61f96ab2/41467_2024_48234_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d46/11087495/82378348a65e/41467_2024_48234_Fig7_HTML.jpg

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