TRANSGENE-MEDIATED AUXIN OVERPRODUCTION IN ARABIDOPSIS - HYPOCOTYL ELONGATION PHENOTYPE AND INTERACTIONS WIT THE THE HY6-1 HYPOCOTYL ELONGATION AND AXR1 AUXIN-RESISTANT MUTANTS
Cp. Romano et al., TRANSGENE-MEDIATED AUXIN OVERPRODUCTION IN ARABIDOPSIS - HYPOCOTYL ELONGATION PHENOTYPE AND INTERACTIONS WIT THE THE HY6-1 HYPOCOTYL ELONGATION AND AXR1 AUXIN-RESISTANT MUTANTS, Plant molecular biology, 27(6), 1995, pp. 1071-1083
Transgenic Arabidopsis thaliana plants constitutively expressing Agrob
acterium tumefaciens tryptophan monooxygenase (iaaM) were obtained and
characterized. Arabidopsis plants expressing iaaM have up to 4-fold h
igher levels of free indole-3-acetic acid (IAA) and display increased
hypocotyl elongation in the light. This result clearly demonstrates th
at excess endogenous auxin can promote cell elongation in a whole plan
t. Interactions of the auxin-overproducing transgenic plants with the
phytochrome-deficient hy6-1 and auxin-resistant axr1-S mutations were
also studied. The effects of auxin overproduction on hypocotyl elongat
ion were not additive to the effects of phytochrome deficiency in the
hy6-1 mutant, indicating that excess auxin does not counteract factors
that limit hypocotyl elongation in hy6-1 seedlings. Auxin-overproduci
ng seedlings are also qualitatively indistinguishable from wild-type c
ontrols in their response to red, far-red, and blue light treatments,
demonstrating that the effect of excess auxin on hypocotyl elongation
is independent of red and blue light-mediated effects. All phenotypic
effects of iaaM-mediated auxin overproduction (i.e. increased hypocoty
l elongation in the light, severe rosette leaf epinasty, and increased
apical dominance) are suppressed by the auxin-resistant axr1-3 mutati
on. The axr1-3 mutation apparently blocks auxin signal transduction si
nce it does not reduce auxin levels when combined with the auxin-overp
roducing transgene.