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Transgenic Arabidopsis thaliana plants harboring the Agrobacterium tumefaciens phytohormone-biosynthetic genes iaaM and iaaH display an altered development indicative of elevated auxin levels. These plants exhibit an increased apical dominance, increased hypocotyl and petiole length and epinastic leaves and cotyledons. In addition, the transgenic plants display the formation of necrotic spots on leaves and bracts in soil and an altered behavior of axillary buds in tissue culture. Despite transcriptional activity of the iaaM and iaaH promoters in the vasculature of root tissue, root development of young iaaM/iaaH transgenic plants is identical to wild type. However, transgenic iaaM/iaaH plants grown under tissue culture conditions for a prolonged period display both vigorous and ectopic root growth. The level of free IAA in the rosette of the iaaM/iaaH transgenic plants is increased approximately 2-fold compared to wild type. The number of cells comprising the vascular tissue in hypocotyls and inflorescence stems of the transgenic plants is reduced and these plants exhibit a reduced basipetal polar auxin transport in the inflorescence stems. This reduced polar auxin transport probably accounts for the rapid auxin effect on the aerial part of the transgenic plants and the late effect on root development. [ABSTRACT FROM AUTHOR]

The Arabidopsis thaliana (L.) Heynh. mutant delayed-dehiscence2-2 (dde2-2) was identified in an En1/Spm1 transposon-induced mutant population screened for plants showing defects in fertility. The dde2-2 mutant allele is defective in the anther dehiscence process and filament elongation and thus exhibits a male-sterile phenotype. The dde2-2 phenotype can be rescued by application of methyl jasmonate, indicating that the mutant is affected in jasmonic acid biosynthesis. The combination of genetic mapping and a candidate-gene approach identified a frameshift mutation in the ALLENE OXIDE SYNTHASE (AOS) gene, encoding one of the key enzymes of jasmonic acid biosynthesis. Expression analysis and genetic complementation of the dde2-2 phenotype by overexpression of the AOS coding sequence confirmed that the male-sterile phenotype is indeed caused by the mutation in the AOS gene. [ABSTRACT FROM AUTHOR]