Abstract

SummaryMutants in rice (Oryza sativa L. cv. japonica) were used to study the role of the cytoskeleton in signal‐dependent morphogenesis. Mutants obtained by gamma ray irradiation were selected that failed to show inhibition of coleoptile elongation by the antimicrotubular drug ethyl‐N‐phenylcarbamate (EPC). The mutation EPC‐Resistant 31 (ER31), isolated from such a screen, caused lethality in putatively homozygous embryos. Heterozygotes exhibited drug resistance, impaired development of crown roots, and characteristic changes in the pattern of cell elongation: cell elongation was enhanced in mesocotyls and leaf sheaths, but inhibited in coleoptiles. The orientation of cortical microtubules changed correspondingly: for etiolated seedlings, compared with the wild‐type, they were more transverse with respect to the long cell axis in mesocotyls and leaf sheaths, but more longitudinal in coleoptiles. In mutant coleoptiles, in contrast to wild‐type, microtubules did not reorient in response to auxin, and their response to microtubule‐eliminating and microtubule‐stabilizing drugs was conspicuously reduced. In contrast, they responded normally to other stimuli such as gibberellins or red light. Auxin sensitivity as assayed by the dose‐response for callus induction did not show any significant differences between wild‐type and mutant. The mutant phenotype is interpreted in terms of an interrupted link between auxin‐triggered signal transduction and microtubule reorientation.

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