Regulatory Hierarchy of Photomorphogenic Loci: Allele-Specific and Light-Dependent lnteraction

Previous studies suggested that the CONSTlTUTlVE PHOTOMORPHOGENIC 7 (COPI) gene product represses photomorphogenic development in darkness and that light signals reverse this action. In this report, we used genetic analysis to investigate the regulatory hierarchical relationship of COPl and the loci encoding the photoreceptors and other signaling components. Our results showed that copl mutations are epistatic to the long hypocotyl mutations hy7, hy2, hy3, and hy4, suggesting that COPl acts downstream of the phytochromes and a blue light receptor. Although epistasis of a putative null cop7-5 mutation over a hy5 mutation implied that COP7 acts downstream of HY5, the same hy5 mutation can suppress the dark photomorphogenic phenotypes (including hypocotyl elongation and cotyledon cellular differentiation) of the weak cop7-6 mutation. This, and other allele-specific interactions between COP 7 and HY5, may suggest direct physical contact of their gene products. In addition, the synthetic lethality of the weak deetiolatedl (detn and Cop7 mutations and the fact that the copl-6 mutation is epistatic to the det7-7 mutation with respect to light control of seed germination and dark-adaptative gene expression suggested that DETT and COP7 may act in the same pathway, with COP7 being downstream. These results, together with previous epistasis studies, support models in which light signals, once perceived by different photoreceptors, converge downstream and act through a common cascade(s) of regulatory steps, as defined by DETT, HY5, COP7, and likely others, to derepress photomorphogenic development.