NaCl-elicited, vacuolar Ca2+ release facilitates prolonged cytosolic Ca2+ signaling in the salt response of Populus euphratica cells. Issue 5 (May 2015)

• Record Type: Journal Article
• Authors: Zhang, Xuan; Shen, Zedan; Sun, Jian; Yu, Yicheng; Deng, Shurong; Li, Zongyun; Sun, Cunhua; Zhang, Jian; Zhao, Rui; Shen, Xin; Chen, Shaoliang
• Is Part Of: Cell calcium. Volume 57:Issue 5/6(2015)
• Page Start: 348
• Page End: 365
• Publication Date: 2015-05
• Subjects: Vacuolar Ca2+ signaling -- IP3 -- cADPR -- Poplar -- Salinity -- SV channel -- Ion flux; Calcium -- Metabolism -- Periodicals; Vertebrates -- Physiology -- Periodicals; Calcium -- Physiological effect -- Periodicals; Cell physiology -- Periodicals; Calcium in the body -- Periodicals; 572.516
• DOI: 10.1016/j.ceca.2015.03.001
• Languages: English
• ISSNs: 0143-4160

Abstract

Graphical abstract: A schematic diagram of the proposed model showing the NaCl-elicited mechanisms involved in vacuolar Ca 2+ release, and the roles of vacuolar-generated Ca 2+ in mediating ionic homeostasis in Populus euphratica cells. Highlights: Vacuolar Ca 2+ signaling networks were established in salt-stressed poplar cells. The salt-induced vacuolar Ca 2+ release depends on eATP, Ca 2+ influx, H2 O2, and NO. NaCl-altered Ca 2+ mobilizations were mediated by IP3 and cADPR but not by SV channel. The salt-elicited vacuolar Ca 2+ release mediates ionic homeostasis in poplar cells. IP3 /cADPR-mediated vacuolar Ca 2+ release enhances salt-responsive genes expression. Abstract: High environmental salt elicits an increase in cytosolic Ca 2+ ([Ca 2+ ]cyt ) in plants, which is generated by extracellular Ca 2+ influx and Ca 2+ release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca 2+ release from vacuoles and its role in ionic homeostasis in Populus euphratica . In vivo Ca 2+ imaging showed that NaCl treatment induced a rapid elevation in [Ca 2+ ]cyt, which was accompanied by a subsequent release of vacuolar Ca 2+ . In cell cultures, NaCl-altered intracellular Ca 2+ mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP3 ) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca 2+ release was dependent on extracellular ATP, extracellular Ca 2+ influx, H2 O2, and NO. In vitro Ca 2+ flux recordings confirmed that IP3, cADPR, and Ca 2+ induced substantial Ca 2+ efflux from intact vacuoles, but this vacuolar Ca 2+ flux did not directly respond to ATP, H2 O2, or NO. Moreover, the IP3 /cADPR-mediated vacuolar Ca 2+ release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K + maintenance, Na + and Cl − exclusion across the plasma membrane, and Na + /H + and Cl − /H + exchanges across the vacuolar membrane.