Browsing by Author "Bailly, Christophe"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Restricted
    ROS production and protein oxidation as a novel mechanism for seed dormancy alleviation.
    (Wiley, 2007) Oracz, Krystyna; Bouteau, Hayat El-Maarouf; Farrant, Jill M; Cooper, Keren; Belghazi, Maya; Job, Claudette; Job, Dominique; Corbineau, Franc¸oise; Bailly, Christophe
    At harvest, sunflower (Helianthus annuus L.) seeds are dormant and unable to germinate at temperatures below 15C. Seed storage in the dry state, known as after-ripening, is associated with an alleviation of embryonic dormancy allowing subsequent germination at suboptimal temperatures. To identify the process by which dormancy is broken during after-ripening, we focused on the role of reactive oxygen species (ROS) in this phenomenon. After-ripening entailed a progressive accumulation of ROS, namely superoxide anions and hydrogen peroxide, in cells of embryonic axes. This accumulation, which was investigated at the cellular level by electron microscopy, occurred concomitantly with lipid peroxidation and oxidation (carbonylation) of specific embryo proteins. Incubation of dormant seeds for 3 h in the presence of hydrogen cyanide (a compound that breaks dormancy) or methylviologen (a ROS-generating compound) also released dormancy and caused the oxidation of a specific set of embryo proteins. From these observations, we propose a novel mechanism for seed dormancy alleviation. This mechanism involves ROS production and targeted changes in protein carbonylation patterns.
  • Thumbnail Image
    Item
    Restricted
    Wheat seedlings as a model to understand desiccation tolerance and sensitivity
    (Wiley, 2004) Farrant, Jill M; Bailly, Christophe; Leymarie, Juliette; Hamman, Brigitte; Côme, Daniel; Corbineau, Franc¸oise
    The coleoptiles of wheat (Triticum aestivum L.) seedlings of cultivar Tre´mie are desiccation tolerant when 3 days old, although the roots are not. Cutting some of the coleoptiles open prior to dehydration rapidly increased the drying rate. This rendered the coleoptiles sensitive to desiccation, providing a useful model with which to study desiccation tolerance. Both sensitive and tolerant seedlings were dehydrated to 0.3 g H2O g 1 dry mass (g.g) and thereafter rehydrated. Sensitive tissues accrued the lipid peroxidation products H2O2 and MDA, and substantial subcellular damage was evident in dry tissues. H2O2 and MDA accumulated slightly only in dry tolerant coleoptiles and no subcellular damage was evident. The activity of antioxidant enzymes glutathione reductase (EC1.6.2.4), superoxide dismutase (EC 1.14.1.1) and catalase (EC 1.11.1.6) increased on drying in both tolerant and sensitive tissues, but were sustained on rehydration in only the tolerant tissues. It is proposed that free radical damage sustained during rapid drying exceeded the ameliorating capacity of antioxidant systems, allowed accrual of lethal subcellular damage. Slow drying enabled sufficient detoxification by antioxidants to minimize damage and allow tolerance to drying. Three LEA- (p11 and Asp 52) and dehydrin- (XV8) like proteins were detected by western blots in tolerant coleoptiles dried to 3.0 g.g and below. Only one (Asp 52) was induced at low water content in rapidly dried sensitive coleoptiles. None were present in root tissues. XV8 RNA (northern analyses) was induced on drying only in tolerant coleoptiles and correlated with protein expression. These putative stress-protein protectants (and XV8 transcripts) appear to be down-regulated during germination but wheat seedlings temporarily retain the ability to reproduce them if drying is slow. Sucrose accumulation during dehydration was similar for both sensitive and tolerant tissues, suggesting that this sugar has little role, or is not effective in isolation, in protecting against desiccation damage in wheat seedlings. In summary, the slower rate at which tolerant coleoptiles were dried allowed for the mobilization of protection mechanisms with which to survive desiccation. Rapid drying of tissues precluded induction of some putative stress protein protectants and caused damage in excess of the ameliorating capacity of the antioxidant protection system.