PubMed1993
Light signals have profound effects on morphogenesis of hypocotyls and cotyledons of Arabidopsis seedlings, but the mechanisms by which light signals are transduced and integrated to control these processes are poorly understood. We report here the identification of a new class of constitutive photomorphogenic (cop) mutants, cop2, cop3, and cop4, in which dark-grown seedlings have open and enlarged cotyledons resembling those of light-grown wild-type seedlings. The epistatic relationships of these three mutations to previously characterized phytochrome-deficient mutations suggest that COP2, COP3, and COP4 may act downstream of phytochrome in the light regulatory pathway. Mutations in each of the three loci alleviate the normal inhibition of cell-type differentiation, cell enlargement, and lateral cell division observed in cotyledons of dark-grown wild-type seedlings, but do not affect plastid differentiation. The cop4 mutation also leads to high-level dark expression of nuclear, but not plastid-encoded, light-inducible genes. We further show that for the nuclear cab1 gene encoding a chlorophyll a/b binding protein of the photosynthetic light-harvesting complex, activation in dark-grown cop4 mutants is achieved by modulation of promoter activity. Interestingly, COP4 modulates cab1 promoter activity through a pathway distinct from that of COP1 and COP9. Furthermore, cop4 mutants are defective in both root and shoot gravitropic responses, indicating that the COP4 locus may be involved in both light-signaling and gravity-sensing processes.