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Accueil > Départements > Biochimie, Biophysique et Biologie Structurale > Diana KIRILOVSKY : Mécanismes régulateurs chez les organismes photosynthétiques

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Articles syndiqués

  • Correction to ’Overexpression of plastid terminal oxidase in Synechocystis sp. PCC 6803 alters cellular redox state’.

    8 novembre, par Feilke K, Ajlani G, Krieger-Liszkay A
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    Correction to 'Overexpression of plastid terminal oxidase in Synechocystis sp. PCC 6803 alters cellular redox state'.

    Philos Trans R Soc Lond B Biol Sci. 2017 Dec 19;372(1736):

    Authors: Feilke K, Ajlani G, Krieger-Liszkay A

    PMID: 29109231 [PubMed - in process]

  • The paralogs to the C-terminal domain of the cyanobacterial OCP are carotenoid donors to HCPs.

    23 septembre, par Muzzopappa F, Wilson A, Yogarajah V, Cot S, Perreau F, Montigny C, Bourcier de Carbon C, Kirilovsky D
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    The paralogs to the C-terminal domain of the cyanobacterial OCP are carotenoid donors to HCPs.

    Plant Physiol. 2017 Sep 21;:

    Authors: Muzzopappa F, Wilson A, Yogarajah V, Cot S, Perreau F, Montigny C, Bourcier de Carbon C, Kirilovsky D

    Abstract
    The photoactive Orange Carotenoid Protein photoprotects cyanobacteria cells by quenching singlet oxygen and excess excitation energy. Its N-terminal domain (NTD) is the active part of the protein and the C-terminal domain (CTD) regulates the activity. Recently, the characteristics of a family of soluble carotenoid-binding proteins (Helical Carotenoid Proteins or HCPs), paralogs of NTD-OCP, were described. Bioinformatics studies also revealed the existence of genes coding for homologs of CTD. Here, we show that the latter genes encode carotenoid proteins (CTDHs). This family of proteins contains two subgroups with distinct characteristics. One CTDH of each clade was further characterized and proved to be very good singlet oxygen quenchers. When synthesized in E. coli or Synechocystis PCC 6803, CTDHs form dimers that share a carotenoid molecule and are able to transfer their carotenoid to apo-HCPs and apo-OCP. The CTDHs from clade 2 have a cysteine in position 103. A disulfide bond is easily formed between the monomers of the dimer preventing carotenoid transfer. This suggests that the transfer of the carotenoid could be redox regulated in clade 2 CTDH. We also demonstrate here that apo-OCPs and apo CTDHs are able to take the carotenoid directly from membranes, while HCPs are unable. HCPs need the presence of CTDH to become holo-proteins. We propose that in cyanobacteria the CTDHs are carotenoid donors to HCPs.

    PMID: 28935842 [PubMed - as supplied by publisher]

  • Carnosic acid and carnosol, two major antioxidants of rosemary, act through different mechanisms.

    17 septembre, par Loussouarn M, Krieger-Liszkay A, Svilar L, Bily A, Birtic S, Havaux M
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    Carnosic acid and carnosol, two major antioxidants of rosemary, act through different mechanisms.

    Plant Physiol. 2017 Sep 15;:

    Authors: Loussouarn M, Krieger-Liszkay A, Svilar L, Bily A, Birtic S, Havaux M

    Abstract
    Carnosic acid, a phenolic diterpene specific of the Lamiaceae family, is highly abundant in rosemary species. Despite numerous industrial and medicinal/pharmaceutical applications of its antioxidative features, this compound in planta and its antioxidant mechanism have received little attention, except a few studies of rosemary plants under natural conditions. In vitro analyses, using HPLC-UV and luminescence imaging, revealed that carnosic acid and its major oxidized derivative, carnosol, protect lipids from oxidation. Both compounds preserved linolenic acid and monogalactosyldiacylglycerol from singlet oxygen and from hydroxyl radical. When applied exogenously, they were both able to protect thylakoid membranes prepared from Arabidopsis leaves against lipid peroxidation. Different levels of carnosic acid and carnosol in two contrasted rosemary varieties correlated with tolerance to lipid peroxidation. Upon ROS oxidation of lipids, carnosic acid was consumed and oxidized into various derivatives, including into carnosol, while carnosol resisted, suggesting that carnosic acid is a chemical quencher of ROS. The antioxidative function of carnosol relies on another mechanism, occurring directly in lipid oxidation process. Under oxidative conditions that did not involve ROS generation, carnosol inhibited lipid peroxidation, contrary to carnosic acid. Using spin probes and EPR detection, we confirmed that carnosic acid, rather than carnosol, is a ROS quencher. Various oxidized derivatives of carnosic acid were detected in rosemary leaves in low light, indicating chronic oxidation of this compound, and accumulated in plants exposed to stress conditions, in parallel with a loss of carnosic acid, confirming that chemical quenching of ROS by carnosic acid takes place in planta.

    PMID: 28916593 [PubMed - as supplied by publisher]

  • Overexpression of plastid terminal oxidase in Synechocystis sp. PCC 6803 alters cellular redox state.

    17 août, par Feilke K, Ajlani G, Krieger-Liszkay A
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    Overexpression of plastid terminal oxidase in Synechocystis sp. PCC 6803 alters cellular redox state.

    Philos Trans R Soc Lond B Biol Sci. 2017 Sep 26;372(1730):

    Authors: Feilke K, Ajlani G, Krieger-Liszkay A

    Abstract
    Cyanobacteria are the most ancient organisms performing oxygenic photosynthesis, and they are the ancestors of plant plastids. All plastids contain the plastid terminal oxidase (PTOX), while only certain cyanobacteria contain PTOX. Many putative functions have been discussed for PTOX in higher plants including a photoprotective role during abiotic stresses like high light, salinity and extreme temperatures. Since PTOX oxidizes PQH2 and reduces oxygen to water, it is thought to protect against photo-oxidative damage by removing excess electrons from the plastoquinone (PQ) pool. To investigate the role of PTOX we overexpressed rice PTOX fused to the maltose-binding protein (MBP-OsPTOX) in Synechocystis sp. PCC 6803, a model cyanobacterium that does not encode PTOX. The fusion was highly expressed and OsPTOX was active, as shown by chlorophyll fluorescence and P700 absorption measurements. The presence of PTOX led to a highly oxidized state of the NAD(P)H/NAD(P)(+) pool, as detected by NAD(P)H fluorescence. Moreover, in the PTOX overexpressor the electron transport capacity of PSI relative to PSII was higher, indicating an alteration of the photosystem I (PSI) to photosystem II (PSII) stoichiometry. We suggest that PTOX controls the expression of responsive genes of the photosynthetic apparatus in a different way from the PQ/PQH2 ratio.This article is part of the themed issue 'Enhancing photosynthesis in crop plants: targets for improvement'.

    PMID: 28808098 [PubMed - in process]

  • Singlet oxygen triggers chloroplast rupture and cell death in the zeaxanthin epoxidase defective mutant aba1 of Arabidopsis thaliana under high light stress.

    15 juillet, par Sánchez-Corrionero Á, Sánchez-Vicente I, González-Pérez S, Corrales A, Krieger-Liszkay A, Lorenzo Ó, Arellano JB

    Singlet oxygen triggers chloroplast rupture and cell death in the zeaxanthin epoxidase defective mutant aba1 of Arabidopsis thaliana under high light stress.

    J Plant Physiol. 2017 Jul 04;216:188-196

    Authors: Sánchez-Corrionero Á, Sánchez-Vicente I, González-Pérez S, Corrales A, Krieger-Liszkay A, Lorenzo Ó, Arellano JB

    Abstract
    The two Arabidopsis thaliana mutants, aba1 and max4, were previously identified as sharing a number of co-regulated genes with both the flu mutant and Arabidopsis cell suspension cultures exposed to high light (HL). On this basis, we investigated whether aba1 and max4 were generating high amounts of singlet oxygen ((1)O2) and activating (1)O2-mediated cell death. Thylakoids of aba1 produced twice as much (1)O2 as thylakoids of max4 and wild type (WT) plants when illuminated with strong red light. (1)O2 was measured using the spin probe 2,2,6,6-tetramethyl-4-piperidone hydrochloride. 77-K chlorophyll fluorescence emission spectra of thylakoids revealed lower aggregation of the light harvesting complex II in aba1. This was rationalized as a loss of connectivity between photosystem II (PSII) units and as the main cause for the high yield of (1)O2 generation in aba1. Up-regulation of the (1)O2 responsive gene AAA-ATPase was only observed with statistical significant in aba1 under HL. Two early jasmonate (JA)-responsive genes, JAZ1 and JAZ5, encoding for two repressor proteins involved in the negative feedback regulation of JA signalling, were not up-regulated to the WT plant levels. Chloroplast aggregation followed by chloroplast rupture and eventual cell death was observed by confocal imaging of the fluorescence emission of leaf cells of transgenic aba1 plants expressing the chimeric fusion protein SSU-GFP. Cell death was not associated with direct (1)O2 cytotoxicity in aba1, but rather with a delayed stress response. In contrast, max4 did not show evidence of (1)O2-mediated cell death. In conclusion, aba1 may serve as an alternative model to other (1)O2-overproducing mutants of Arabidopsis for investigating (1)O2-mediated cell death.

    PMID: 28709027 [PubMed - as supplied by publisher]

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