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NMT作為生命科學底層核心技術(shù)，是建立活體創(chuàng)新科研平臺的*技術(shù)。2005年~2020年，NMT已扎根中國15年。2020年，中國NMT銷往瑞士蘇黎世大學，正式打開歐洲市場。

研究使用平臺：NMT植物耐鹽創(chuàng)新科研平臺

期刊：Molecular Plant

主題：Na⁺流為SOS調(diào)控植物耐鹽新機制研究提供證據(jù)

標題：ESCRT-I component VPS23A sustains salt tolerance by strengthening the SOS module in Arabidopsis

影響因子：12.084

檢測指標：Na⁺流速

檢測樣品：擬南芥根部分生區(qū)

Na⁺流實驗處理方法：

12日齡的擬南芥在150 mM NaCl處理5h

Na+流實驗測試液成份：

0.1 mM CaCl₂, 0.1 mM KCl, 0.5 mM NaCl, and 0.3 mM MES，pH5.8

作者：謝旗、郭巖、于菲菲、婁麗娟

中文摘要

含鈉轉(zhuǎn)運蛋白SOS1和調(diào)節(jié)蛋白SOS2和SOS3的鹽分過度敏感（SOS）信號模塊，*是幫助植物抵抗鹽分積累的中央鹽分排泄系統(tǒng)。

在這里我們報告說，VPS23A是運輸所需的內(nèi)體分選復合物（ESCRT）的組成部分，在SOS模塊賦予植物耐鹽性的功能中起著至關(guān)重要的作用。VPS23A增強了SOS2 / SOS3復合體的相互作用。

在存在鹽脅迫的情況下，VPS23A積極調(diào)節(jié)SOS2向質(zhì)膜的重新分布過程，然后激活SOS1的反轉(zhuǎn)運蛋白活性以減少植物細胞中的Na+積累。遺傳證據(jù)表明，通過SOS2和SOS3的過表達實現(xiàn)的耐鹽性取決于VPS23A。兩者合計，我們的結(jié)果表明，VPS23A是SOS模塊的關(guān)鍵調(diào)節(jié)因子，可影響SOS2在細胞膜上的亞細胞定位。

此外，膜結(jié)合的SOS2賦予擬南芥幼苗較強的耐鹽性，揭示了SOS2分選對細胞膜發(fā)揮作用的重要性。

(D and E)Net Na+ fluxes in root tips. Non-invasive Micro-test Technology (NMT) was used for Na+ flux measurement in vivo. 10-day-old seedlings cultured in liquid ½MS medium were treated with 0 (D, upper panel) or 150 mM NaCl (D, lower panel) for 5 h, and then the continuous transient Na+ fluxes were recorded for about 6 min. Each point is the mean of four individual plants (D). Quantitative analysis of the means of net Na+ fluxes within the continuous period of 0–6 min as shown in (E).The values are means ± SD of three independent repeats. *P value <0.05.

英文摘要

Salt-Overly-Sensitive (SOS) signaling module comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3, is well known as the central salt excretion system that helps plants against salt accumulation.

Here we report that VPS23A, a component of the endosomal sorting complex required for transport (ESCRT), plays an essential role in the function of the SOS module to confer plant salt tolerance. VPS23A enhances the interaction of the SOS2/SOS3 complex.

In the presence of salt stress, VPS23A positively regulates the process of re-distribution of SOS2 to the plasma membrane and then activates the antiporter activity of SOS1 to reduce Na+ accumulation in plant cells. Genetic evidence  demonstrated that salt tolerance achieved by the overexpression of SOS2 and SOS3 depended on VPS23A. Taken together, our results identified that VPS23A is a crucial regulator of the SOS module that affects the subcellular localization of SOS2 to the cell membrane.

Moreover, the strong salt tolerance of Arabidopsis seedlings conferred by a membrane-bound SOS2 revealed the significance of the action of SOS2 sorting to the cell membrane in achieving its function.