A mutation in tobacco (Nicotiana tabacum L. cv `Xanthi') called lat (low auxin transport) that changes many morphogenic features throughout the life of the plant has been isolated. Abnormalities were observed in seed development, embryogenesis, cotyledon formation, leaf initiation and development, leaf veination pattern, and flower development. Selfed R2 lat mutant plants set between 60% and 90% fewer seeds than wild-type tobacco, and about 10% of these seeds did not germinate. Non-germinating seeds contained either abnormal embryos or abnormal endosperm tissues. There was no uniformity in the stage at which embryonic development ceased in the aberrant seeds. Seedlings often revealed abnormal and highly varied phenotypes after germination. In some of these cases, cotyledons were heart-shaped, fused, cup-shaped, or cylindrical. Leaf morphology ranged from normal to cup-shaped, and some leaves occasionally produced shoots from the leaf midvein. Flowers ranged from normal to compound with occasional fused floral parts or split petals. Stamens were sometimes petal-like. This unusual assortment of phenotypic changes suggested that the mutation might affect a basic component of plant metabolism. We found that polar transport of indole-3-acetic acid (IAA) was reduced to about 9-19% of the wild-type level in the inflorescence axis of selfed R2 lat mutants. In addition, supplementation of 1-naphthaleneacetic acid (NAA) to sterile media suppressed some of the abnormalities of the lat mutation so long as the plants grew there. Similarities in the phenotype of embryos, cotyledon and leaf shapes, translocation of labeled IAA, and response to applied NAA indicate that the lat locus of tobacco may be analogous to the pin locus of Arabidopsis, or produce a protein that functions in the same auxin-transport pathway.
Keywords: Auxin transport; Indole acetic acid; Key words Tobacco; Mutation; Nicotiana tobacum.