| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
We examined whether Aux/IAA proteins, which are key players in auxin-signal transduction, are involved in brassinosteroid (BR) responses. Iaa7laxr2-1 and iaal7laxr3-3 mutants showed aberrant BR sensitivity and aberrant BR-induced gene expression, which were observed organ-dependently. Two auxin inhibitors were tested in terms of BR responses. Yokonolide B inhibited BR responses, whereas p-Chlorophenoxyisobutyric acid did not inhibit BR responses. DNA microarray analysis revealed that 108 genes were up-regulated, while only eight genes were down-regulated in iaa7. Among the genes that were up-or down-regulated in axr2, 22% were BL-inducible genes, 20% were auxin-inducible genes, and the majority were sensitive neither to BR nor to auxin. An inhibitor of BR biosynthesis, brassinazole, inhibited auxin induction of DR5-GUS gene, which is consisted of a synthetic Auxin-Response Element, a minimum promoter, and a β-glucuronidase. These results suggest that the Aux/IAA proteins function in auxin-and BR-signaling pathways, and that the IAA proteins function as the signaling components modulating BR sensitivity in a manner dependent on organ type.
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