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Aucuba japonica ‘Variegata’ is a widely used ornamental shrub with green-yellow variegated leaves. In this study, the formation of leaf variegation and photosynthetic characteristics in green and yellow sectors were investigated. There were no marked anatomical differences in tissue organization between the green and yellow sectors. At the cellular level, it was observed that the chloroplasts in the yellow leaf tissue were vacuolated. Besides, the pigment contents of the yellow leaf tissue were obviously lower than those in the green areas, and a very low intensity of chlorophyll auto-fluorescence was generated from the yellow areas. Furthermore, significantly lower values of F 0 , F m , F v /F m , Ф PSII and non-photochemical quenching (NPQ) were noticed in yellow sectors compared to the green ones, indicating that the yellow leaf tissue was less photoprotected than the green area. In addition, the yellow sectors showed lower net photosynthesis and dark respiration rates compared to the green leaf tissue. Immunofluorescence showed large amounts of ribulose-1, 5-bisphosphate carboxylase/oxygenase (Rubisco) in green leaf tissue, while only faint fluorescence was detected in the yellow sectors. As a whole, the results of this study suggest that the leaf variegation of A. japonica ‘Variegata’ is “pigment type” and that this pigment-related leaf variegation affects photosynthetic light use in the variegated leaves. These findings also shed light on the coloration mechanism of ornamental plant foliage. [ABSTRACT FROM AUTHOR]

In the photosynthetic apparatus, a major target of photodamage is the D1 reaction center protein of photosystem II (PSII). Photosynthetic organisms have developed a PSII repair cycle in which photodamaged D1 is selectively degraded. A thylakoid membrane-bound metalloprotease, FtsH, was shown to play a critical role in this process. Here, the effect of FtsHs in D1 degradation was investigated in Arabidopsis (Arabidopsis thaliana) mutants lacking FtsH2 (yellow variegated2 [var2]) or FtsH5 (van). Because these mutants are characterized by variegated leaves that sometimes complicate biochemical studies, we employed another mutation,fu-gaeri1 (fug1), that suppresses leaf variegation in van and var2 to examine D1 degradation. Two- dimensional blue native PAGE showed that var2 has less PSII supercomplex and more PSII intermediate lacking CP43, termed RC47, than the wild type under normal growth light. Moreover, our histochemical and quantitative analyses revealed that chloroplasts in var2 accumulate significant levels of reactive oxygen species, such as superoxide radical and hydrogen peroxide. These results indicate that the lack of FtsH2 leads to impaired D1 degradation at the step of RC47 formation in PSII repair and to photooxidative stress even under nonphotoinhibitory conditions. Our in vivo D1 degradation assays, carried out by nonvariegated var2 fug1 and var1 fug1 leaves, demonstrated that D1 degradation was impaired in different light conditions. Taken together, our results suggest the important role of chloroplastic FtsHs, which was not precisely examined in vivo. Attenuated D1 degradation in the nonvariegated mutants also suggests that leaf variegation seems to be independent of the PSII repair. [ABSTRACT FROM AUTHOR]

Variegated plants typically have green- and white-sectored leaves. Cells in the green sectors contain normal-appearing chloroplasts, whereas cells in the white sectors lack pigments and appear to be blocked at various stages of chloroplast biogenesis. Variegations can be caused by mutations in nuclear, chloroplast or mitochondrial genes. In some plants, the green and white sectors have different genotypes, but in others they have the same (mutant) genotype. One advantage of variegations is that they provide a means of studying genes for proteins that are important for chloroplast development, but for which mutant analysis is difficult, either because mutations in a gene of interest are lethal or because they do not show a readily distinguishable phenotype. This paper focuses on Arabidopsis variegations, for which the most information is available at the molecular level. Perhaps the most interesting of these are variegations caused by defective nuclear gene products in which the cells of the mutant have a uniform genotype. Two questions are of paramount interest: (1) What is the gene product and how does it function in chloroplast biogenesis? (2) What is the mechanism of variegation and why do green sectors arise in plants with a uniform (mutant) genotype? Two paradigms of variegation mechanism are described: immutans ( im) and variegated2 ( var2). Both mechanisms emphasize compensating activities and the notion of plastid autonomy, but redundant gene products are proposed to play a role in var2, but not in im. It is hypothesized that threshold levels of certain activities are necessary for normal chloroplast development. [ABSTRACT FROM AUTHOR]