Physiological studies with excised stem segments have implicated the plant hormone indole-3-acetic acid (IAA or auxin) in the regulation of cell elongation. Supporting evidence from intact plants has been somewhat more difficult to obtain, however. Here, we report the identification and characterization of an auxin-mediated cell elongation growth response in Arabidopsis thaliana. When grown in the light at high temperature (29°C), Arabidopsis seedlings exhibit dramatic hypocotyl elongation compared with seedlings grown at 20°C. This temperature-dependent growth response is sharply reduced by mutations in the auxin response or transport pathways and in seedlings containing reduced levels of free IAA. In contrast, mutants deficient in gibberellin and abscisic acid biosynthesis or in ethylene response are unaffected. Furthermore, we detect a corresponding increase in the level of free IAA in seedlings grown at high temperature, suggesting that temperature regulates auxin synthesis or catabolism to mediate this growth response. Consistent with this possibility, high temperature also stimulates other auxin-mediated processes including auxin-inducible gene expression. Based on these results, we propose that growth at high temperature promotes an increase in auxin levels resulting in increased hypocotyl elongation. These results strongly support the contention that endogenous auxin promotes cell elongation in intact plants.Plant growth and development are regulated by both external environmental factors, such as light quantity and quality, and by a set of endogenous regulators collectively known as the phytohormones. In many instances, these two sets of determinants interact with one another. For example, phytohormones mediate many of the stress responses that facilitate adaptation to environmental changes. One of the most studied examples of this occurs during periods of drought stress, when the phytohormone abscisic acid mediates stomatal pore closure, resulting in reduced transpirational water loss (1).The Arabidopsis hypocotyl is a useful model for investigating the regulation of plant growth. Hypocotyl elongation in Arabidopsis is the result of regulated cell expansion that is under both environmental and hormonal controls (2). In the absence of light, seedlings undergo skotomorphogenic development. The cotyledons remain closed, an apical hook is formed, and the hypocotyl becomes greatly elongated. Light induces the photomorphogenic developmental program resulting in cotyledon expansion, leaf development, the initiation of photosynthesis, and limited hypocotyl growth. In addition to light, all of the known plant hormones have been implicated in the control of hypocotyl elongation. Brassinosteroids, auxin, and gibberellins (GAs) promote hypocotyl growth, whereas cytokinins and abscisic acid (ABA) have growth inhibitory effects (3-7).Ethylene both positively and negatively regulates hypocotyl elongation. In darkness, ethylene inhibits elongation, but at least under some conditions in the light, ethylene prom...

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uses a variant Bt Cry3Bb1 insecticidal protein (Donovan et al., 1992). Cry3Bb1 is known to be biologically active The corn rootworm (CRW; Diabrotica spp.) is one of the most against several species within the Coleopteran family serious pests of corn in the USA. Chemical insecticides and crop rotation have been the only two options available to growers for Chrysomelidae, including the western corn rootworm, managing CRW. Unfortunately, both of these tactics can be ineffective Diabrotica virgifera virgifera LeConte (Rupar et al., as a result of either resistance or behavioral modifications. In this 1991). The biological activity of this protein against D. paper, we describe transgenic maize (Zea mays L.) hybrids that control virgifera virgifera suggested its potential use in creating CRW. These hybrids were created with a Cry3Bb1 Bacillus thurintransgenic plants expressing Cry3Bb1 that would confer giensis (Bt) variant that is approximately eight times more lethal to protection to corn root tissue from larval feeding damcorn rootworm larvae than the wild-type protein. A DNA vector age. To further augment protection of the root system containing the modified cry3Bb1 gene was placed under control of a from larval feeding damage, modifications were introroot-enhanced promoter (4-AS1) and was introduced into embryonic duced in the cry3Bb1 gene that gave rise to an amino acid maize cells by microprojectile bombardment. Described here is the variant Cry3Bb1 protein with an eight-fold increase in molecular genetic characterization, protein expression levels, and field performance of the recently commercialized MON863 hybrids.

Transgenic Arabidopsis thaliana plants constitutively expressing Agrobacterium tumefaciens tryptophan monooxygenase (iaaM) were obtained and characterized. Arabidopsis plants expressing iaaM have up to 4-fold higher levels of free indole-3-acetic acid (IAA) and display increased hypocotyl elongation in the light. This result clearly demonstrates that excess endogenous auxin can promote cell elongation in a whole plant. Interactions of the auxin-overproducing transgenic plants with the phytochrome-deficient hy6-1 and auxin-resistant axr1-3 mutations were also studied. The effects of auxin overproduction on hypocotyl elongation 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-overproducing seedlings are also qualitatively indistinguishable from wild-type controls 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 hypocotyl elongation in the light, severe rosette leaf epinasty, and increased apical dominance) are suppressed by the auxin-resistant axr1-3 mutation. The axr1-3 mutation apparently blocks auxin signal transduction since it does not reduce auxin levels when combined with the auxin-overproducing transgene.