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

Abstract

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.

Inducible transgenic tobacco system to study the mechanisms underlying chlorosis mediated by the silencing of chloroplast heat shock protein 90

“…Although the downregulation of Hsp90C was clearly demonstrated in the report, they also demonstrated that various vd-sRNAs were produced in the infected plants and could target other host genes. Therefore, their conclusion, although quite reasonable, relies on the findings in A. thaliana mutants [30]. We generated a conditional silencing system for Hsp90C in tobacco and demonstrated that the silencing of Hsp90C alone leads plants to chlorosis, supporting the notion that Hsp90C silencing plays a major role in PLMVd pathogenesis.…”

“…One may claim that the leaf twisting and shrinking phenotypes observed in the Dex-treated transgenic lines might be due to off-target effects of the induced expression of Hsp90C-hpRNA. This notion is unlikely because, firstly, we selected carefully the target region for hpRNA construction to include only the Hsp90C-specific region, which is not found in Hsp90 proteins located in different subcellular compartments, and secondly, developmental defects were reported in null mutants and co-suppression lines of A. thaliana [17,30].…”

“…Moreover, we have previously suggested that PR1a induction during Tav-mediated chlorosis is independent of SA. Because Hsp90C is known to be involved in chloroplast biogenesis and retrograde signaling in A. thaliana and Chlamydomonas reinhardtti [6,30,33,34], an unknown SA-independent signaling from the affected chloroplast may have a role in the regulation of the PR1a nuclear gene. On the other hand, higher production of ROS is anticipated in malfunctioning chloroplasts of Hsp90C-silenced plants [36].…”

“…4, 5). The morphological changes in Hsp90C-silenced lines could be attributed to an impaired chloroplast function resulted from the RNA silencing of Hsp90C genes, because developmental defects have been reported in Arabidopsis thaliana Hsp90C mutants and Hsp90C co-suppressed lines [17,18,30].…”

Plastids unleashed: their development and their integration in plant development

“…When light is unavailable or insufficient, as is often the case in cotyledons of germinating seedlings or exceptionally in young leaf cells, proplastids accumulate large amounts of thylakoid lipids with the complex of protochlorophyllide and a form of the enzyme responsible for its light-driven reduction, protochlorophyllide reductase A (Armstrong et al, 1995;Vinti et al, 2005). Such plastids are called etioplasts, as dark-grown seedlings are said to be etiolated ( Fig.…”