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Effects of the axr2 mutation of Arabidopsis on cell shape in hypocotyl and inflorescence

The axr2 mutation of Arabidopsis thaliana (L.) Heynh. confers resistance to the plant growth hormones auxin, ethylene and abscisic acid. In addition, mutant plants have a pronounced dwarf phenotype and display defects in both shoot and root gravitopism. To further characterize this mutant we have de...

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Bibliographic Details
Published in:Planta 1992-09, Vol.188 (2), p.271-278
Main Authors: Timpte, C.S, Wilson, A.K, Estelle, M
Format: Article
Language:English
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Summary:The axr2 mutation of Arabidopsis thaliana (L.) Heynh. confers resistance to the plant growth hormones auxin, ethylene and abscisic acid. In addition, mutant plants have a pronounced dwarf phenotype and display defects in both shoot and root gravitopism. To further characterize this mutant we have determined the phenotype of both dark- and light-grown mutant seedlings. We find that the height of axr2 hypocotyls is reduced in dark conditions compared with wild-type seedlings and that both dark- and light-grown hypocotyls have a gravitropic defect. In addition, we have examined the cellular anatomy of a variety of wild-type and axr2 tissues using light and scanning electron microscopy. Our results indicate that the axr2 mutation has a dramatic effect on cell length in both the inflorescence and the hypocotyl and a lesser effect on cell number in these tissues. The largest difference was observed in the epidermis of the inflorescence where axr2 cells were approximately eightfold shorter than wild-type cells. We suggest that these reductions in cell length and number are sufficient to explain most aspects of the axr2 phenotype. In addition, we propose that a reduction in auxin-mediated cell elongation is responsible for the gravitropic defect in mutant roots, hypocotyls and floral stems. Finally, we have found that the reduction in epidermal cell size in the mutant inflorescence is accompanied by a fourfold increase in stoma density. The implications of this result for models of stoma development are discussed.
ISSN:0032-0935
1432-2048
DOI:10.1007/bf00216824