Romano C P, Robson P R, Smith H, Estelle M, Klee H
Monsanto Agricultural Group, St. Louis, MO 63198, USA.
Plant Mol Biol. 1995 Mar;27(6):1071-83. doi: 10.1007/BF00020881.
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.
获得并鉴定了组成型表达根癌农杆菌色氨酸单加氧酶（iaaM）的转基因拟南芥植株。表达iaaM的拟南芥植株游离吲哚 - 3 - 乙酸（IAA）水平高达野生型的4倍，且在光照下下胚轴伸长增加。这一结果清楚地表明，过量的内源生长素能够促进整株植物的细胞伸长。同时也研究了生长素过量产生的转基因植株与缺乏光敏色素的hy6 - 1和抗生长素的axr1 - 3突变体之间的相互作用。在hy6 - 1突变体中，生长素过量产生对下胚轴伸长的影响与光敏色素缺乏的影响并非相加关系，这表明过量的生长素不会抵消限制hy6 - 1幼苗下胚轴伸长的因素。在对红光、远红光和蓝光处理的反应中，生长素过量产生的幼苗在定性上与野生型对照也没有区别，这表明过量生长素对下胚轴伸长的影响独立于红光和蓝光介导的效应。iaaM介导的生长素过量产生的所有表型效应（即光照下下胚轴伸长增加、莲座叶严重向下弯曲以及顶端优势增强）都被抗生长素的axr1 - 3突变所抑制。axr1 - 3突变显然阻断了生长素信号转导，因为当它与生长素过量产生的转基因结合时，并不会降低生长素水平。
