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

Summary 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 SUPERROOT 2 ( CYP 83B1), 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 BR s caused adventitious roots from hypocotyls, indicative of an increased response to BR s 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 BR s in promoting growth in Arabidopsis at the level of their biosynthetic enzymes.