Dendrobium flower buds and flowers have an abscission zone at the base of the pedicel (flower stalk). Ethylene treatment of cv. Miss Teen inflorescences induced high rates of abscission in flower buds but did not affect abscission once the flowers had opened. It is not known if auxin is a regulator of the abscission of floral buds and open flowers. The hypotheses that auxin is such a regulator and is responsible for the decrease in ethylene sensitivity were tested. Severed inflorescences bearing 4–8 floral buds and 4–6 open flowers were used in all tests. The auxin antagonists 2,3,5-triiodobenzoic acid (TIBA, an inhibitor of auxin transport) or 2-(4-chlorophenoxy)-2-methyl propionic acid (CMPA, an inhibitor of auxin action) were applied to the stigma of open flowers. Both chemicals induced high flower abscission rates, even if the inflorescences were not treated with ethylene. The effects of these auxin antagonists virtually disappeared when the inflorescences were treated with 1-methylcyclopropene (1-MCP), indicating that the abscission induced by the auxin antagonists was due to ethylene. Removal of the open flowers at the distal end of the pedicel hastened the time to abscission of the remaining pedicel, and also resulted in an increase in ethylene sensitivity. Indole-3-acetic acid (IAA) in lanolin, placed on the cut surface of the pedicel, replaced the effect of the removed flower. Treatments that promoted abscission of open flowers up-regulated a gene encoding a β-1,4-glucanase (Den-Cel1) in the abscission zone (AZ). The abundance of Den-Cel1 mRNA was highly correlated with β-1,4-glucanase activity in the AZ. The results show that auxin is an endogenous regulator of floral bud and flower abscission and suggest that auxin might explain, at least partially, why pedicel abscission of Dendrobium cv. Miss Teen changes from very ethylene-sensitive to ethylene-insensitive.