title: H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.
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+)](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. 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+)](cyt), 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+)](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 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.
authors.affiliation: College of Biological Sciences and Technology, Beijing Forestry University, Beijing 100083, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Sun
authors.forename: Mei-Juan
authors.initials: MJ
authors.lastname: Wang
authors.forename: Ming-Quan
authors.initials: MQ
authors.lastname: Ding
authors.forename: Shu-Rong
authors.initials: SR
authors.lastname: Deng
authors.forename: Mei-Qin
authors.initials: MQ
authors.lastname: Liu
authors.forename: Cun-Fu
authors.initials: CF
authors.lastname: Lu
authors.forename: Xiao-Yang
authors.initials: XY
authors.lastname: Zhou
authors.forename: Xin
authors.initials: X
authors.lastname: Shen
authors.forename: Xiao-Jiang
authors.initials: XJ
authors.lastname: Zheng
authors.forename: Zeng-Kai
authors.initials: ZK
authors.lastname: Zhang
authors.forename: Jin
authors.initials: J
authors.lastname: Song
authors.forename: Zan-Min
authors.initials: ZM
authors.lastname: Hu
authors.forename: Yue
authors.initials: Y
authors.lastname: Xu
authors.forename: Shao-Liang
authors.initials: SL
authors.lastname: Chen
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D020013:Calcium Signaling / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism*; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism*; D006706:Homeostasis / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000378:metabolism* / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D032107:Populus / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011522:Protons; D011523:Protoplasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D013312:Stress, Physiological / Q000187:drug effects*; D014638:Vanadates / Q000494:pharmacology
chemical_list: D011522:Protons; D014638:Vanadates; D012965:Sodium Chloride; D000584:Amiloride; D012964:Sodium; D006861:Hydrogen Peroxide; D011188:Potassium