Calcium release from the endoplasmic reticulum of higher plants elicited by the NADP metabolite nicotinic acid adenine dinucleotide phosphate
Calcium release from the endoplasmic reticulum of higher plants elicited by the NADP metabolite nicotinic acid adenine dinucleotide phosphate
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NADP 代谢物烟酸腺嘌呤二核苷酸磷酸引起的高等植物内质网钙释放
DOI：
10.1073/pnas.140217897
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发表时间：
2000-07-18
影响因子：
11.1
通讯作者：
Sanders, D
中科院分区：
文献类型：
--
作者：
Navazio, L;Bewell, MA;Sanders, D
高等植物和动物一样对钙离子动员剂1，4，5-三磷酸肌醇（InsP（3））和环ADP-核糖（cADPR）有反应。本研究通过使用囊泡Ca-45（2+）通量测定，我们证明红甜菜和花椰菜的微粒体囊泡也对烟酸腺嘌呤二核苷酸磷酸（NAADP）有反应，NAADP是最近在海洋无脊椎动物中描述的一种Ca 2+释放分子。NAADP从红甜菜非液泡来源的微粒体中有效地动员Ca 2+，K-1/2 = 96 nM。蔗糖梯度分离的花椰菜微粒体的分析表明，NAADP敏感的Ca 2+池来自内质网。NAADP敏感的Ca 2+通路的这种唯一的非空泡定位使其与InsP（3）和cADPR门控通路区分开来。脱敏实验表明，来自花椰菜组织的匀浆中含有低水平的NAADP（125 pmol/mg），并在NAADP合成时与底物NADP和烟酸提供主管。NAADP诱导的Ca 2+释放对肝素和8-NH 2-cADPR不敏感，肝素和8-NH 2-cADPR分别是InsP（3）和cADPR控制机制的特异性抑制剂。然而. NAADP诱导的Ca 2+释放可以通过用阈下剂量的NAADP预处理来阻断，如先前在海胆卵中所观察到的。此外，NAADP门控的Ca 2+释放途径不依赖于胞质游离Ca 2+，因此不能操作Ca 2+诱导的Ca 2+释放。与海胆系统相反，植物中NAADP门控的Ca 2+释放途径不被L型通道拮抗剂阻断。植物细胞内存在多种Ca ~（2+）动员途径和Ca ~（2+）释放位点，这可能有助于产生刺激特异性Ca ~（2+）信号。
Higher plants share with animals a responsiveness to the Ca2+ mobilizing agents inositol 1,4,5-trisphosphate (InsP(3)) and cyclic ADP-ribose (cADPR). In this study. by using a vesicular Ca-45(2+) flux assay, we demonstrate that microsomal vesicles from red beet and cauliflower also respond to nicotinic acid adenine dinucleotide phosphate (NAADP), a Ca2+-releasing molecule recently described in marine invertebrates. NAADP potently mobilizes Ca2+ with a K-1/2 = 96 nM from microsomes of nonvacuolar origin in red beet. Analysis of sucrose gradient-separated cauliflower microsomes revealed that the NAADP-sensitive Ca2+ pool was derived from the endoplasmic reticulum. This exclusively nonvacuolar location of the NAADP-sensitive Ca2+ pathway distinguishes it from the InsP(3)-and cADPR-gated pathways. Desensitization experiments revealed that homogenates derived from cauliflower tissue contained low levels of NAADP (125 pmol/mg) and were competent in NAADP synthesis when provided with the substrates NADP and nicotinic acid. NAADP-induced Ca2+ release is insensitive to heparin and 8-NH2-cADPR, specific inhibitors of the InsP(3)- and cADPR-controlled mechanisms, respectively. However. NAADP-induced Ca2+ release could be blocked by pretreatment with a subthreshold dose of NAADP, as previously observed in sea urchin eggs. Furthermore, the NAADP-gated Ca2+ release pathway is independent of cyto solic free Ca2+ and therefore incapable of operating Ca2+-induced Ca2+ release. In contrast to the sea urchin system, the NAADP-gated Ca2+ release pathway in plants is not blocked by L-type channel antagonists. The existence of multiple Ca2+ mobilization pathways and Ca2+ release sites might contribute to the generation of stimulus-specific Ca2+ signals in plant cells.