Search

Abstract: The Arabidopsis vte1 mutant is devoid of tocopherol and plastochromanol (PC‐8). When exposed to excess light energy, vte1 produced more singlet oxygen (1O2) and suffered from extensive oxidative damage compared with the wild type. Here, we show that overexpressing the solanesyl diphosphate synthase 1 (SPS1) gene in vte1 induced a marked accumulation of total plastoquinone (PQ‐9) and rendered the vte1 SPS1oex plants tolerant to photooxidative stress, indicating that PQ‐9 can replace tocopherol and PC‐8 in photoprotection. High total PQ‐9 levels were associated with a noticeable decrease in 1O2 production and higher levels of Hydroxyplastoquinone (PQ‐C), a 1O2‐specific PQ‐9 oxidation product. The extra PQ‐9 molecules in the vte1 SPS1oex plants were stored in the plastoglobules and the chloroplast envelopes, rather than in the thylakoid membranes, whereas PQ‐C was found almost exclusively in the thylakoid membranes. Upon exposure of wild‐type plants to high light, the thylakoid PQ‐9 pool decreased, whereas the extrathylakoid pool remained unchanged. In vte1 and vte1 SPS1oex plants, the PQ‐9 losses in high light were strongly amplified, affecting also the extrathylakoid pool, and PQ‐C was found in high amounts in the thylakoids. We conclude that the thylakoid PQ‐9 pool acts as a 1O2 scavenger and is replenished from the extrathylakoid stock. [ABSTRACT FROM AUTHOR]

Summary: Prenylquinols (tocochromanols and plastoquinols) serve as efficient physical and chemical quenchers of singlet oxygen (1O2) formed during high light stress in higher plants. Although quenching of 1O2 by prenylquinols has been previously studied, direct evidence for chemical quenching of 1O2 by plastoquinols and their oxidation products is limited in vivo. In the present study, the role of plastoquinol‐9 (PQH2‐9) in chemical quenching of 1O2 was studied in Arabidopsis thaliana lines overexpressing the SOLANESYL DIPHOSPHATE SYNTHASE 1 gene (SPS1oex) involved in PQH2‐9 and plastochromanol‐8 biosynthesis. In this work, direct evidence for chemical quenching of 1O2 by plastoquinols and their oxidation products is presented, which is obtained by microscopic techniques in vivo. Chemical quenching of 1O2 was associated with consumption of PQH2‐9 and formation of its various oxidized forms. Oxidation of PQH2‐9 by 1O2 leads to plastoquinone‐9 (PQ‐9), which is subsequently oxidized to hydroxyplastoquinone‐9 [PQ(OH)‐9]. We provide here evidence that oxidation of PQ(OH)‐9 by 1O2 results in the formation of trihydroxyplastoquinone‐9 [PQ(OH)3‐9]. It is concluded here that PQH2‐9 serves as an efficient 1O2 chemical quencher in Arabidopsis, and PQ(OH)3‐9 can be considered as a natural product of 1O2 reaction with PQ(OH)‐9. The understanding of the mechanisms underlying 1O2 chemical quenching provides information on the role of plastoquinols and their oxidation products in the response of plants to photooxidative stress. [ABSTRACT FROM AUTHOR]

Abstract: Light and cytokinins are known to be the key players in the regulation of plant senescence. In detached leaves, the retarding effect of light on senescence is well described; however, it is not clear to what extent is this effect connected with changes in endogenous cytokinin levels. We have performed a detailed analysis of changes in endogenous content of 29 cytokinin forms in detached leaves of Arabidopsis thaliana (wild‐type and 3 cytokinin receptor double mutants). Leaves were kept under different light conditions, and changes in cytokinin content were correlated with changes in chlorophyll content, efficiency of photosystem II photochemistry, and lipid peroxidation. In leaves kept in darkness, we have observed decreased content of the most abundant cytokinin free bases and ribosides, but the content of cis‐zeatin increased, which indicates the role of this cytokinin in the maintenance of basal leaf viability. Our findings underscore the importance of light conditions on the content of specific cytokinins, especially N6‐(Δ2‐isopentenyl)adenine. On the basis of our results, we present a scheme summarizing the contribution of the main active forms of cytokinins, cytokinin receptors, and light to senescence regulation. We conclude that light can compensate the disrupted cytokinin signalling in detached leaves. [ABSTRACT FROM AUTHOR]