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Heterostyly distinct hermaphroditic floral morphs enforce outbreeding. Morphs differ structurally, promote cross-pollination, and physiologically block self-fertilization. In <i>Turnera</i> the self-incompatibility (S)-locus controlling heterostyly possesses three genes specific to short-styled morph genomes. Only one gene, <i>TsBAHD</i>, is expressed in pistils and this has been hypothesized to possess brassinosteroid (BR)-inactivating activity. We tested this hypothesis using heterologous expression in <i>Arabidopsis thaliana</i> as a bioassay, thereby assessing growth phenotype, and the impacts on the expression of endogenous genes involved in BR homeostasis and seedling photomorphogenesis. Transgenic <i>A. thaliana</i> expressing <i>TsBAHD</i> displayed phenotypes typical of BR-deficient mutants, with phenotype severity dependent on <i>TsBAHD</i> expression level. <i>BAS1</i>, which encodes an enzyme involved in BR inactivation, was downregulated in <i>TsBAHD</i>-expressing lines. <i>CPD</i> and <i>DWF,</i> which encode enzymes involved in BR biosynthesis, were upregulated. Hypocotyl growth of <i>TsBAHD</i> dwarfs responded to application of brassinolide in light and dark in a manner typical of plants over-expressing genes encoding BR-inactivating activity. These results provide empirical support for the hypothesis that TsBAHD possesses BR-inactivating activity. Further this suggests that style length in <i>Turnera</i> is controlled by the same mechanism (BR inactivation) as that reported for <i>Primula</i>, but using a different class of enzyme. This reveals interesting convergent evolution in a biochemical mechanism to regulate floral form in heterostyly.