Arabidopsis cue mutants with defective plastids are impaired primarily in the photocontrol of expression of photosynthesis-associated nuclear genes.

Plant photoreceptors detect light cues and initiate responses ranging from chloroplast differentiation to the control of morphogenesis and flowering. The photocontrol of photosynthesis-related nuclear genes appears closely related to 'retrograde plastid signals' by which the status of the organelle controls the expression of nuclear genes. However, what specific role, if any, plastid-originated signals play in light responses is poorly understood: it has in the past been proposed that plastid signals play a role in all responses to 'high fluence' far-red light perceived by the light-labile phytochrome A, irrespective of whether they involve photosynthesis-related genes. To explore this further, we have re-examined the phenotype of three cue (cab-underexpressed) Arabidopsis mutants, defective in chloroplast development. The mutants have underdeveloped etioplasts, with increasing impairments in cue6, cue8 and cue3. The mutants show only small defects in photocontrol of hypocotyl elongation and cotyledon opening under prolonged far-red or red light, and normal photocontrol under blue. On the other hand, the expression of photosynthesis-associated nuclear genes is much more impaired in the mutants in the dark and following red or far-red light short treatments or continuous light, than that of those phytochrome-dependent genes tested which are not associated with photosynthesis. Furthermore, red/far-red photoreversible responses involving photosynthesis-related genes (induction of Lhcb1-cab promoter activity, and photoreversible extent of greening) mediated by phytochrome B and other photo-stable phytochromes, both show a reduction in the cue mutants, which correlates with the etioplast defect. Our evidence demonstrates that plastid-derived signals need to be operational in order for the phytochrome control of photosynthetic nuclear genes to occur.