The dumpy (dpy) mutant of tomato (Lycopersicon esculentum Mill.) exhibits short stature, reduced axillary branching, and altered leaf morphology. Application of brassinolide and castasterone rescued the dpy phenotype, as did C-23-hydroxylated, 6-deoxo intermediates of brassinolide biosynthesis. The brassinolide precursors campesterol, campestanol, and 6-deoxocathasterone failed to rescue, suggesting that dpy may be affected in the conversion of 6-deoxocathasterone to 6-deoxoteasterone, similar to the Arabidopsis constitutive photomorphogenesis and dwarfism (cpd) mutant. Measurements of endogenous brassinosteroid levels by gas chromatography-mass spectrometry were consistent with this hypothesis. To examine brassinosteroid-regulated gene expression in dpy, we performed cDNA subtractive hybridization and isolated a novel xyloglucan endotransglycosylase that is regulated by brassinosteroid treatment. The curl-3 (cu-3) mutant (Lycopersicon pimpinellifolium [Jusl.] Mill.) shows extreme dwarfism, altered leaf morphology, de-etiolation, and reduced fertility, all strikingly similar to the Arabidopsis mutant brassinosteroid insensitive 1 (bri1). Primary root elongation of wild-type L. pimpinellifolium seedlings was strongly inhibited by brassinosteroid application, while cu-3 mutant roots were able to elongate at the same brassinosteroid concentration. Moreover, cu-3 mutants retained sensitivity to indole-3-acetic acid, cytokinins, gibberellin, and abscisic acid while showing hypersensitivity to 2,4-dichlorophenoxyacetic acid in the root elongation assay. The cu-3 root response to hormones, coupled with its bri1-like phenotype, suggests that cu-3 may also be brassinosteroid insensitive.