The Tryptophan Conjugates of Jasmonic and Indole-3-Acetic Acids Are Endogenous Auxin Inhibitors

被引:152
作者
Staswick, Paul E. [1 ]
机构
[1] Univ Nebraska, Dept Agron & Hort, Lincoln, NE 68583 USA
基金
美国国家科学基金会;
关键词
ARABIDOPSIS-THALIANA; PLANT-GROWTH; METHYL JASMONATE; GENE-EXPRESSION; RESISTANT MUTANTS; ROOT GRAVITROPISM; TRANSPORT; PROTEIN; FAMILY; METABOLISM;
D O I
10.1104/pp.109.138529
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Most conjugates of plant hormones are inactive, and some function to reduce the active hormone pool. This study characterized the activity of the tryptophan (Trp) conjugate of jasmonic acid (JA-Trp) in Arabidopsis (Arabidopsis thaliana). Unexpectedly, JA-Trp caused agravitropic root growth in seedlings, unlike JA or nine other JA-amino acid conjugates. The response was dose dependent from 1 to100 mu M, was independent of the COI1 jasmonate signaling locus, and unlike the jasmonate signal JA-isoleucine, JA-Trp minimally inhibited root growth. The Trp conjugate with indole-3-acetic acid (IAA-Trp) produced a similar response, while Trp alone and conjugates with benzoic and cinnamic acids did not. JA-Trp and IAA-Trp at 25 mu M nearly eliminated seedling root inhibition caused by 2 mu M IAA. The TIR1 auxin receptor is required for activity because roots of tir1-1 grew only approximately 60% of wild-type length on IAA plus JA-Trp, even though tir1-1 is auxin resistant. However, neither JA-Trp nor IAA-Trp interfered with IAA-dependent interaction between TIR1 and Aux/IAA7 in cell-free assays. Trp conjugates inhibited IAA-stimulated lateral root production and DR5-b-glucuronidase gene expression. JA-deficient mutants were hypersensitive to IAA and a Trp-overaccumulating mutant was less sensitive, suggesting endogenous conjugates affect auxin sensitivity. Conjugates were present at 5.8 pmol g(-1) fresh weight or less in roots, seedlings, leaves, and flowers, and the values increased approximately 10-fold in roots incubated in 25 mu M Trp and IAA or JA at 2 mu M. These results show that JA-Trp and IAA-Trp constitute a previously unrecognized mechanism to regulate auxin action.
引用
收藏
页码:1310 / 1321
页数:12
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