Overexpression of a putative Arabidopsis BAHD acyltransferase causes dwarfism that can be rescued by brassinosteroid.

Plant growth and development are ensured through networks of complex regulatory schemes. Genetic approaches have been invaluable in dissecting these regulatory pathways. This study reports the isolation of a semi-dominant dwarf mutant designated abnormal shoot1-1 dominant (abs1-1D) through an Arabidopsis T-DNA activation tagging mutant screen. It was shown that the overexpression of a novel BAHD family acyltransferase gene, ABS1/At4g15400, was the cause of the dwarf phenotype in abs1-1D. Overexpression of ABS1 led to many phenotypic features reminiscent of brassinosteroid (BR) deficient or signalling mutants, and it was shown that exogenously applied BR could effectively rescue the dwarf phenotype of abs1-1D. Furthermore, genetic analyses indicated that abs1-1D interacted, in different ways, with the BR-deficient mutant det2-1, the constitutive BR response mutant bes1-D and the photomorphogenic mutant phyB-1. Moreover, ABS1 expression was activated by BR treatment or in a bes1-D mutant background. Genome-wide transcriptome profiling of abs1-1D revealed clear reprogramming of metabolic pathways, and it was demonstrated that BR biosynthesis genes were activated in abs1-1D and that the flavonoid biosynthesis pathway was repressed in abs1-1D, as well as in det2-1. This work provides new insights into the possible involvement of BAHD acyltransferase in the regulation of plant growth and development, and indicates a possible role of ABS1 in maintaining BR homeostasis.