期刊
PLANT SCIENCE
卷 175, 期 1-2, 页码 161-167出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.plantsci.2008.01.002
关键词
Arabidopsis; ACC synthase; ethylene; etr1-1 mutant; gene expression; GUS reporter
1-Aminocyclopropane-1-carboxylate synthase (ACC synthase, ACS) (S-adenosyl-L-methionine methylthioadenosine-lyase; EC 4.4.1.14), the key enzyme for ethylene biosynthesis, is subjected to positive or negative feedback regulation by the hormone itself. We have previously described, aided by promoter-GUS (beta-glucuronidase) reporter approach, that among members of the multigene family of Arabidopsis ACC synthase, AtACS4, AtACS5 and AtACS7 genes exhibit different responses to exogenous ethylene treatment. Here we report differences in their developmental expression profiles and hormone responses between wild type and etr1-1 mutants. It was found that these three ACS members were all actively expressed in 2-week-old wild type light-grown seedlings but exhibited different profiles in etr1-1 mutant. The expression of AtACS7::GUS during the entire life cycle of Arabidopsis was greatly suppressed in etr1-1 mutant while the expressions of AtACS4:: GUS and AtACS5:: GUS exhibited no significant changes. The effects of seven major plant hormones and ethylene precursor ACC on the promoter activities of these three ACS genes were studied by fluorometric GUS activity assay. It was found that exogenous treatment of IAA, ACC, ABA or JA increased the promoter activity of AtACS4 in the wild type background but the promotions by ACC, ABA and JA were almost absent in the etr1-1 background. Block of the ethylene signaling also abolished both the IAA- and the ABA-induced AtACS5::GUS expression. The ACS7 promoter was responsive to six members of the eight hormones (GA(3), ACC, ABA, JA, SA and BR), among which, the increases by GA3, ACC, SA and BR were abolished in the etrl-1 mutant. Based on these results, the role of ethylene signaling in regulating responses of AtACS4, AtACS5 and AtACS7 to different hormones was discussed. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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