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胡楊細(xì)胞在鹽脅迫下與K+/Na+動(dòng)態(tài)平衡調(diào)控相關(guān)的信號(hào)通路研究

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    近日,北京林業(yè)大學(xué)生物科學(xué)與技術(shù)學(xué)院陳少良實(shí)驗(yàn)室利用“非損傷微測(cè)技術(shù)”取得的科研成果在《Plant, Cell & Environment》(2008 IF 4.666)雜志發(fā)表。這項(xiàng)成果將非損傷微測(cè)技術(shù)與激光共聚焦、X射線微量分析等技術(shù)相結(jié)合,研究了胡楊細(xì)胞在鹽脅迫下與K+/Na+動(dòng)態(tài)平衡調(diào)控相關(guān)的信號(hào)通路,發(fā)現(xiàn)質(zhì)膜H+偶聯(lián)轉(zhuǎn)運(yùn)體(PM H+-coupled transport system)可以激發(fā)H2O2及胞質(zhì)Ca2+信號(hào),進(jìn)而通過調(diào)節(jié)K+通道及Na+/H+反向轉(zhuǎn)運(yùn)體調(diào)控K+/Na+動(dòng)態(tài)平衡。非損傷微測(cè)技術(shù)在本研究中是獲得離子跨膜流動(dòng)信息的必不可少的工具。
      陳少良實(shí)驗(yàn)室在一年多時(shí)間里利用非損傷微測(cè)技術(shù)已經(jīng)連續(xù)發(fā)表三篇高水平的研究論文,達(dá)到甚至超過國(guó)外相同領(lǐng)域的科研水平,躋身世界一流實(shí)驗(yàn)室行列。該實(shí)驗(yàn)室已經(jīng)積累了應(yīng)用非損傷微測(cè)技術(shù)的豐富經(jīng)驗(yàn),培養(yǎng)出以本文第一作者孫。ㄒ彩乔皟善芯空撐牡牡谝蛔髡撸榇淼囊慌炀氄莆辗菗p傷微測(cè)技術(shù)的優(yōu)秀學(xué)子,相信不久還會(huì)有大量的優(yōu)質(zhì)成果誕生。

北京林業(yè)大學(xué)生物科學(xué)與技術(shù)學(xué)院陳少良教授簡(jiǎn)介

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ABSTRACT:

Using confocal microscopy, X-ray microanalysis and the scanning ion-selective electrode technique, we investigated the signalling of H2O2, cytosolic Ca2+ ([Ca2+]cyt) and the
PM H+-coupled transport system in K+/Na+ homeostasis control in NaCl-stressed calluses of Populus euphratica.An obvious Na+ /H+ antiport was seen in salinized cells;however, NaCl stress caused a net K+ efflux, because of the salt-induced membrane depolarization. H2O2 levels, regulated upwards by salinity, contributed to ionic homeostasis,because H2O2 restrictions by DPI or DMTU caused enhanced K+ efflux and decreased Na+ /H+ antiport activity. NaCl induced a net Ca2+ influx and a subsequent rise of [Ca2+]cyt, which is involved in H2O2-mediated K+/Na+ homeostasis in salinized P. euphratica cells. When callus cells were pretreated with inhibitors of the Na+ /H+ antiport system, the NaCl-induced elevation of H2O2 and [Ca2+]cyt was correspondingly restricted, leading to a greater K+ efflux and a more pronounced reduction in Na+ /H+ antiport activity. Results suggest that the PM H+-coupled transport system mediates H+ translocation and triggers the stress signalling of H2O2 and Ca2+, which results in a K+/Na+ homeostasis via mediations of K+ channels and the Na+ /H+ antiport system in the PM of NaCl-stressed cells. Accordingly, a salt stress signalling pathway of P. euphratica cells is proposed.

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