Hormonal interactions in the control of Arabidopsis hypocotyl elongation

The Arabidopsis hypocotyl, together with hormone mutants and chemical inhib itors, was used to study the role of auxin iri cell elongation and its poss ible interactions with ethylene and gibberellin. When wild-type Arabidopsis seedlings were grown on media containing a range of auxin concentrations, hypocotyl growth was inhibited. However, when axr1-12 and 35S-iaaL (which h ave reduced auxin response and levels, respectively) were grown in the same conditions, auxin was able to promote hypocotyl growth. In contrast, auxin does not promote hypocotyl growth of axr3-1, which has phenotypes that sug gest an enhanced auxin response. These results are consistent with the hypo thesis that auxin levels in the wild-type hypocotyl are optimal for elongat ion and that additional auxin is inhibitory. When ethylene responses were r educed using either the ethylene-resistant mutant etr1 or aminoethoxyvinylg lycine, an inhibitor of ethylene synthesis, auxin responses were unchanged, indicating that auxin does not inhibit hypocotyl elongation through ethyle ne. To test for interactions between auxin and gibberellin, auxin mutants w ere grown on media containing gibberellin and gibberellin mutants were grow n on media containing auxin. The responses were found to be the same as wil d-type Arabidopsis seedlings in all cases. In addition, 1 muM of the auxin transport inhibitor 1-naphthylphthalmic acid does not alter the response of wild-type seedlings to gibberellin. Double mutants were made between gibbe rellin and auxin mutants and the phenotypes of these appear additive. These results indicate that auxin and gibberellin are acting independently in hy pocotyl elongation. Thus auxin, ethylene, and gibberellin each regulate hyp ocotyl elongation independently.