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质膜 H+偶联转运系统触发的 H2O2 和胞质 Ca2+信号介导 NaCl 胁迫下胡杨细胞的 K+/Na+稳态。

H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.

机构信息

College of Biological Sciences and Technology, Beijing Forestry University, Beijing 100083, China.

出版信息

Plant Cell Environ. 2010 Jun;33(6):943-58. doi: 10.1111/j.1365-3040.2010.02118.x. Epub 2010 Jan 15.

DOI:10.1111/j.1365-3040.2010.02118.x
PMID:20082667
Abstract

Using confocal microscopy, X-ray microanalysis and the scanning ion-selective electrode technique, we investigated the signalling of H(2)O(2), cytosolic Ca(2+) (Ca(2+)) 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. H(2)O(2) levels, regulated upwards by salinity, contributed to ionic homeostasis, because H(2)O(2) restrictions by DPI or DMTU caused enhanced K(+) efflux and decreased Na(+)/H(+) antiport activity. NaCl induced a net Ca(2+) influx and a subsequent rise of Ca(2+), which is involved in H(2)O(2)-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 H(2)O(2) and Ca(2+) 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 H(2)O(2) and Ca(2+), 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.

摘要

利用共聚焦显微镜、X 射线微量分析和扫描离子选择性电极技术,我们研究了 H2O2、胞质 Ca2+(Ca2+)信号和 PM H+-偶联转运系统在 NaCl 胁迫下胡杨愈伤组织 K+/Na+稳态控制中的信号转导。在盐化细胞中观察到明显的 Na+/H+反向转运;然而,由于盐诱导的膜去极化,NaCl 胁迫导致净 K+外排。H2O2 水平受盐度调节而上调,有助于离子稳态,因为 DPI 或 DMTU 对 H2O2 的限制导致增强的 K+外排和降低的 Na+/H+反向转运活性。NaCl 诱导净 Ca2+内流和随后的 Ca2+升高,这与盐化胡杨细胞中 H2O2 介导的 K+/Na+稳态有关。当愈伤组织细胞用 Na+/H+反向转运系统抑制剂预处理时,NaCl 诱导的 H2O2 和 Ca2+升高相应受到限制,导致更大的 K+外排和更明显的 Na+/H+反向转运活性降低。结果表明,PM H+-偶联转运系统介导 H+转运,并触发 H2O2 和 Ca2+的应激信号,通过 PM 中的 K+通道和 Na+/H+反向转运系统介导,导致 NaCl 胁迫细胞的 K+/Na+稳态。因此,提出了胡杨细胞的盐胁迫信号通路。

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