Aluminum-induced secretion of organic acid by cowpea (Vigna unguiculata L.) roots
文献类型: 外文期刊
第一作者: Yu, Li
作者: Yu, Li;Guo, Shirong;Yan, Jun;Zhu, Weimin
作者机构:
关键词: Aluminum;Cowpea;Malate;Anion-channel inhibitors;Protein-synthesis inhibitors
期刊名称:SCIENTIA HORTICULTURAE ( 影响因子:3.463; 五年影响因子:3.672 )
ISSN: 0304-4238
年卷期: 2012 年 135 卷
页码:
收录情况: SCI
摘要: Cowpea (Vigna unguiculata L cv. Lulutong 1) is a leguminous vegetable which is well adapted to infertile acid soil. The mechanisms of aluminum (Al) resistance in cowpea are poorly understood. This study aimed to analyze the possible Al resistance mechanisms of cowpea. After exposure to Al. both malate and citrate were secreted from cowpea roots, but the secretion of these organic acids was not specific to Al. Potassium (P) starvation also induced the secretion of malate and citrate. The secretion of malate was the dominant response to Al stress. Exposure to 50 mu M La3+ (Lanthanum) did not induce organic acid secretion. Secretion of organic acid was detected after 3-6 h exposure to Al, and increased significantly after 6 h exposure, which suggested that this plant showed a pattern II-type organic acid secretion. This is supported by the finding that a protein-synthesis inhibitor, cycloheximide (CHM), significantly inhibited secretion. Two types of anion-channel inhibitors had different effects on Al-induced secretion of organic acids, 9-anthracene carboxylic acid (A-9-C), which completely inhibited secretion whereas niflumic acid (NIF) had no effect. In the presence of A-9-C, Al inhibited root elongation more significantly. Compared with the control, the root tips showed no significant change in organic acid content or in citrate synthase (CS), malate dehydrogenase (MDH) and succinate dehydrogenase (SDH) activities. Taken together, these results indicated that the secretion of malate played a dominant role in the response to Al stress by cowpea plants. The secretion pattern was type II, and protein synthesis might be involved in the secretion process. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.
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