Axillary bud growth is inhibited by auxin produced at the shoot apex and transported down the stem. Removal of the shoot apex by decapitation can release buds from inhibition, and application of auxin to the cut stump can restore bud inhibition. However auxin action is likely to be indirect because auxin does not accumulate in inhibited buds, and therefore requires a second messenger. The max4 mutant of Arabidopsis has increased b,ud growth that leads to increased branching in mature plants. The axillary buds of isolated nodes are also partially resistant to exogenous auxin applied to the apical cut stump. The max4 mutation also partially rescues the branch!ng of the axr3-1 auxin over-responding mutant. The auxin resistant phenotype of the max4 mutant appears to be specific to bud growth because max4 seedlings were only slightly resistant to exogenous auxin, and the max4 mutation did not rescue other auxin related phenotypes of the Bxr3-1 mutant. The phenotype and auxin physiology of the max4 mutant is reminiscent of the/amosus pea mutants. The ramosus1 mutant regulates a graft transmissible signal that interacts with auxin to inhibit bud growth. The max4 and ramosus1 mutant phenotypes are caused by mutations in orthologous genes, encoding a member of the polyene dioxygenase family. All of the family members characterised to date function around a carbon-carbon double bond of polyene chain compounds with cyclic carbon end groups. MAX4 is most related to animal polyene dioxygenases that cleave carotenoid substrates. Possibly the MAX4/RMS1 proteins cleave a carotenoid to produce a novel mobile signal that iFlhibits bud growth, and may act as an auxin second messenger.