Plant morphogenesis depends on accurate control over growth anisotropy. To learn to what extent the control of growth anisotropy depends on cellular metabolism, we surveyed the response of growing roots to a range of inhibitors. Seedlings of Arabidopsis thaliana L. (Heynh), 7-8 d old, were transplanted onto plates containing an inhibitor, and elongation and radial expansion of roots were measured over the subsequent 2-d period. Fourteen inhibitors of diverse metabolic processes inhibited root elongation but failed to stimulate radial expansion. These inhibitors were aluminum sulfate, aphidicolin (DNA synthesis), caffeine (cell-plate formation), cisplatin (DNA synthesis), cycloheximide (protein synthesis), 3,4-dehydro-L-proline (proline hydroxylation), 6-dimethylaminopurine (protein kinases), dinitrophenol (mitochondrial ATP synthesis), galactose (UDP-glucose formation), Lovastatin, formerly mevinolin (isoprenoid formation), methionine sulfoximine (glutamine synthetase), methotrexate (folate metabolism), XRD-489 (synthesis of branched-chain amino acids), and high or low calcium treatments. These results show that various types of metabolic disruption, although inhibitory to elongation, do not reduce the high degree of anisotropic growth of the root. However, five chemicals did stimulate radial expansion; namely, the detergent, digitonin; two inhibitors of vesicle secretion, monensin and brefeldin A; and two inhibitors of actomyosin, cytochalasin B and butanedione monoxime. The maximum radial expansion induced by these compounds (except butanedione monoxime) was greater than that caused by ethylene, and the morphology of treated roots did not resemble that of roots treated with ethylene. These results indicate that vesicle secretion and actomyosin play a role in controlling anisotropic expansion.