The Arabidopsis dep1 and dep2 mutations act synergistically to alter phytochrome-regulated growth responses

Caihong Qiu^1,2 and Timothy Short¹

¹Queens College, ²Graduate Center, The City University of New York, NY

A genetic screen of Arabidopsis thaliana seedlings yielded a series of mutants that display slightly longer hypocotyls under white light than those of wild type. Two of the complementation groups, designated dep1 and dep2 for deficient photomorphogenesis, showed marginally longer hypocotyls than those of the wild type under continuous white light, red light, and far-red light. Although their apical hooks open in all light regimes, a greater proportion of the cotyledons remained appressed under these light conditions. Both mutants exhibit slightly delayed flowering times in long days compared with that of wild type. Neither dep1 nor dep2 mutants exhibit any detectable abnormal phenotype in darkness, indicating that the deficiencies are light dependent.

Double mutants harboring both dep1 and dep2 exhibit much more pronounced phenotypic deficiencies, more comparable to those of a phyA null mutant with respect to germination, hypocotyl elongation, cotyledon opening in far-red light, far-red-induced anthocyanin accumulation, far-red-preconditioned greening responses and late flowering. The dep1 and dep2 single mutants and the double mutant exhibit normal levels of phytochrome A apoprotein, and the receptors apparently bind chromophore as they undergo normal light-dependent degradation.

However, extracts of the double mutant may contain reduced amounts of spectrally active phytochrome. Furthermore, the dep mutants show additional deficiencies more characteristic of phyB pathway mutants, including loss of red-dependent gravitropic sensitivity and longer hypocotyls in red light. Therefore, Dep1 and Dep2 play pleiotropic roles in signaling downstream of multiple phytochromes. The synergistic effects observed in the double mutants suggest either partial redundancy or parallel pathways at work at this stage of phytochrome signaling.