Abstract
Emerging evidence suggests that individual members of the phytochrome family of photoreceptors may regulate discrete facets of plant photomorphogenesis. We report here the isolation of phytochrome A mutants of Arabidopsis using a novel screening strategy aimed at detecting seedlings with long hypocotyls in prolonged far-red light. Complementation analysis of 10 selected mutant lines showed that each represents an independent, recessive allele at a new locus, designated hy8. Immunoblot and spectrophotometric analyses of two of these lines, hy8-1 and hy8-2, showed that, whereas phytochromes B and C are expressed at wild-type levels, phytochrome A is undetectable, thus indicating that the long hypocotyl phenotype displayed by these mutants is caused by phytochrome A deficiency. A third allele, hy8-3, expresses wild-type levels of spectrally normal phytochrome A, suggesting a mutation that has resulted in loss of biological activity in an otherwise photochemically active photoreceptor molecule. Together with physiological experiments, these data provide direct evidence that endogenous phytochrome A is responsible for the "far-red high irradiance response" of etiolated seedlings, but does not play a major role in mediating responses to prolonged red or white light. Because the hy8 and the phytochrome B-deficient hy3 mutants exhibit reciprocal responsivity toward prolonged red and far-red light, respectively, the evidence indicates that phytochromes A and B have distinct photosensory roles in regulating seedling development.