Why hypocotyl extension mutants need to be characterized at the cell level: a case study of axr3-1

Since the discovery of auxin, a debate has taken place as to whether the auxin distribution in elongat-ing organs can account for the distinctive cell elongation pro®les that have been found. In an attempt to address this important issue, the elonga-tion pro®les of cells have been compared in the hypocotyls of wild-type and auxin-hypersensitive axr3-1 Arabidopsis Columbia ecotype seedlings. Clear differences in cell elongation pro®les were found in the two types of seedling, whether they were light- or dark-grown. However, it was not pos-sible unambiguously to ascribe the cell elongation pro®le differences to the proposition that the axr3-1 mutation causes the hypocotyl to be hypersensitive to auxin. The possibility that the abnormal hypocotyl elongation pro®le of the mutant was a secondary effect, consequent on a more fundamental effect of the axr3-1 mutation, is considered. It is clear from this study that cell elongation and its control needs to be studied at the cell, and not the organ, level. To characterize a mutant as having a short, or long, hypocotyl is inadequate. To determine which factors control the timing and the magnitude of cell elonga-tion requires the demonstration of correlations between the growth rate of cells and their content of regulating substances or their sensitivity to that substance. Studies of the cell elongation pro®les of the many hypocotyl length mutants could also be a very effective means of probing the co-ordination of root and shoot elongation