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Abstract Although numerous physiological studies have addressed the interactions between brassinosteroids and auxins, little is known about the underlying molecular mechanisms. Using an Affymetrix GeneChip representing approximately 8,300 Arabidopsis genes, we studied comprehensive transcript profiles over 24 h in response to indole-3-acetic acid (IAA) and brassinolide (BL). We identified 409 genes as BL inducible, 276 genes as IAA inducible, and 637 genes in total. These two hormones regulated only 48 genes in common, suggesting that most of the actions of each hormone are mediated by gene expression that is unique to each. IAA-up-regulated genes were enriched in genes regulated in common. They were induced quickly by IAA and more slowly by BL, suggesting divergent physiological roles. Many were early auxin-inducible genes and their homologs, namely SAUR, GH3, and IAA. The comprehensive comparison also identified IAA- and BL-specific genes, which should help to elucidate the specific actions of each hormone. The identified genes were classified using hierarchical clustering based on the similarity of their responses to the two hormones. Gene classification also allowed us to analyze the frequency of cis-elements. The TGTCTC element, a core element of the previously reported auxin response element, was not enriched in genes specifically regulated by IAA but was enriched in the 5′-flanking region of genes up-regulated by both IAA and BL. Such gene classification should be useful for predicting the functions of unknown genes, to understand the roles of these two hormones, and the promoter analysis should provide insight into the interaction of transcriptional regulation by the two hormones.
The inhibitory properties of a first synthetic jasmonic acid biosynthesis inhibitor, JM‐8686, were investigated. Steady‐state kinetic analysis indicates that the compound is a competitive inhibitor of allene oxide synthase (AOS) with a K i value of approximate 0.62 ± 0.15 μM. Dialysis experiment indicates that AOS inactivation by JM‐8686 is reversible. The optical difference spectroscopy analysis of JM‐8686 and AOS interaction indicates that JM‐8686 induced type II binding spectra with a K d value of approximate 1.6 ± 0.2 μM, suggesting that JM‐8686 binds to the prosthetic heme iron of AOS. Comparison of the inhibitory potency of the compound against HPL (CYP74B) from tomato revealed that JM‐8686 was a highly selective inhibitor for AOS.
Brassinosteroids (BRs) are plant hormones that regulate plant development and environmental response. Brz-insensitive-long hypocotyl4 (BIL4) was identified as a positive regulator of BR signaling that interacts with the BR receptor, BRASSINOSTEROID INSENSITIVE 1 (BRI1), and inhibits vacuolar degradation of BRI1 in Arabidopsis thaliana. Although BIL4 also localizes to the vacuolar membrane, the possible vacuolar function of BIL4 remains unknown. Here, we studied the effect of BIL4 and BR signaling on vacuole shape in root meristem cells using genetic and pharmacological approaches. In BIL4-deficient plants, vacuoles assumed a smaller luminal structure. Treatment with brassinolide (BL), the most active BR, resulted in visibly larger vacuoles, whereas treatment with the BR biosynthesis inhibitor Brz resulted in substantially smaller luminal vacuolar structures. In the bri1 mutant, vacuolar shapes exhibited small and fragmented structures. Our results suggest that BR signaling impacts vacuolar shape.
Limited information is available concerning the interactions between the brassinosteroid (BR) and auxin signaling pathways. The expression pattern of the SAUR-AC1 gene, an early auxin-inducible gene in Arabidopsis, was studied in response to brassinolide (BL), in the presence of a BR-biosynthesis inhibitor, in a BR-deficient mutant, and in combination with auxin. The results suggested that the SAUR-AC1 gene is regulated by BRs independently of auxin levels, and that it is important in BR-mediated elongation. The axr1 (auxin insensitive 1) mutant was less sensitive to BL-induced elongation and BL-induced SAUR-AC1 expression, suggesting that a ubiquitin ligase-mediated system is involved in BR-mediated elongation.
