Arabidopsis gulliver1/superroot2-7 identifies a metabolic basis for auxin and brassinosteroid synergy

Phytohormone homeostasis is essential for proper growth and development of plants. To understand the growth mechanisms mediated by hormonal levels, we isolated a gulliver1 (gul1) mutant that had tall stature in the presence of both brassinazole and the light. The gul1 phenotype depended on functional BR biosynthesis; the genetic introduction of dwarf4, a BR biosynthetic mutation, masked the long hypocotyl phenotype of gul1. Furthermore, BR biosynthesis was dramatically enhanced, such that the level of 22-hydroxy campesterol was 5.8-fold greater in gul1. Molecular cloning revealed that gul1 was a missense mutation, resulting in a glycine to arginine change at amino acid 116 in SUPERROOT2 (CYP83B1), which converts indole acetaldoxime to an S-alkyl thiohydroximate adduct in the indole glucosinolate pathway. Auxin metabolite profiling coupled with quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis of auxin biosynthetic genes revealed that gul1/sur2-7 activated multiple alternative branches of tryptophan-dependent auxin biosynthetic pathways. Furthermore, exogenous treatment of gul1/sur2-7 with BRs caused adventitious roots from hypocotyls, indicative of an increased response to BRs relative to wild-type. Different from severe alleles of sur2, gul1/sur2-7 lacked high-auxin' phenotypes that include stunted growth and callus-like disintegration of hypocotyl tissues. The auxin level in gul1/sur2-7 was only 1.6-fold greater than in the wild-type, whereas it was 4.2-fold in a severe allele like sur2-8. Differences in auxin content may account for the range of phenotypes observed among the sur2 alleles. This unusual allele provides long-sought evidence for a synergistic interaction between auxin and BRs in promoting growth in Arabidopsis at the level of their biosynthetic enzymes.