近日，北京林業(yè)大學生物科學與技術學院陳少良實驗室利用“非損傷微測技術”取得的科研成果在《Plant, Cell & Environment》（2008 IF 4.666）雜志發(fā)表。這項成果將非損傷微測技術與激光共聚焦、X射線微量分析等技術相結合，研究了胡楊細胞在鹽脅迫下與K⁺/Na⁺動態(tài)平衡調控相關的信號通路，發(fā)現(xiàn)質膜H⁺偶聯(lián)轉運體（PM H⁺-coupled transport system）可以激發(fā)H₂O₂及胞質Ca²⁺信號，進而通過調節(jié)K⁺通道及Na⁺/H⁺反向轉運體調控K⁺/Na⁺動態(tài)平衡。非損傷微測技術在本研究中是獲得離子跨膜流動信息的必不可少的工具。
      陳少良實驗室在一年多時間里利用非損傷微測技術已經(jīng)連續(xù)發(fā)表三篇高水平的研究論文，達到甚至超過國外相同領域的科研水平，躋身世界一流實驗室行列。該實驗室已經(jīng)積累了應用非損傷微測技術的豐富經(jīng)驗，培養(yǎng)出以本文第一作者孫�。ㄒ彩乔皟善�研究論文的第一作者）為代表的一批熟練掌握非損傷微測技術的優(yōu)秀學子，相信不久還會有大量的優(yōu)質成果誕生。

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.