Remobilization of leaf S compounds and senescence in response to restricted sulphate supply during the vegetative stage of oilseed rape are affected by mineral N availability

The impact of sulphur limitation on the remobilization of endogenous S compounds during the rosette stage of oilseed rape, and the interactions with N availability on these processes, were examined using a long-term 34SO42− labelling method combined with a study of leaf senescence progression (using SAG12/Cab as a molecular indicator) and gene expression of the transporters, BnSultr4;1 and BnSultr4;2, involved in vacuolar sulphate efflux. After 51 d on hydroponic culture at 0.3 mM 34SO42− (1 atom% excess), the labelling was stopped and plants were subject for 28 d to High S-High N (HS-HN, control), Low S-High N (LS-HN) or Low S-Low N (LS-LN) conditions. Compared with the control, LS-HN plants showed delayed leaf senescence and, whilst the shoot growth and the foliar soluble protein amounts were not affected, S, 34S, and SO42− amounts in the old leaves declined rapidly and were associated with the up-regulation of BnSultr4;1. In LS-LN plants, shoot growth was reduced, leaf senescence was accelerated, and the rapid S mobilization in old leaves was accompanied by decreased 34S and SO42−, higher protein mobilization, and up-regulation of BnSultr4;2, but without any change of expression of BnSultr4;1. The data suggest that to sustain the S demand for growth under S restriction (i) vacuolar SO42− is specifically remobilized in LS-HN conditions without any acceleration of leaf senescence, (ii) SO42− mobilization is related to an up-regulation of BnSultr4;1 and/or BnSultr4;2 expression, and (iii) the relationship between sulphate mobilization and up-regulation of expression of BnSultr4 genes is specifically dependent on the N availability

Dynamics of stable isotope ratios (d13c and d15n) in different organs of crassostrea gigas at two contrasted ecosystems : insights from growth and food sources

International audienceWe studied the influence of food availability on the growth (whole body and organs) of the oyster Crassostrea gigas and on the dynamics of their delta C-13 and delta N-15 respective values. Juvenile oysters originating from Arcachon Bay were transplanted to two contrasting ecosystems, Baie des Veys (BDV) and Rade de Brest (RDB), for a 1-yr growth survey. In BDV, chlorophyll-a concentrations ([Chl-a]) was 3 times higher than in RDB on average, which accounts for the differences in oyster growth between BDV and RDB. Differences in trophic conditions could also explain the differences in C/N ratios and delta C-13 values between sites partly due to higher investment in gametogenesis for the oysters in BDV than in RDB; these differences widened when lipid normalized delta C-13 values were used. Oysters clearly selected microalgae as the main food source, and especially phytoplankton. Gi (Gills), Mu (Muscle) and Re (remaining organs) clearly exhibited different isotopic enrichment levels, with delta(Mu) > delta(Gi) > delta(Re) regardless of C or N elements, culture sites and seasons. delta N-15 discrimination between organs was rather equivalent between sites. These results would benefit from an experiment under controlled conditions along a calibration of the lipid normalization to correct delta C-13 values in bivalves

Seasonal dynamics of trophic relationships between benthic suspension feeders within Crassostrea gigas culture areas.

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The B1-agonist [des-Arg10]-kallidin activates transcription factor NF-kappaB and induces homologous upregulation of the bradykinin B1-receptor in cultured human lung fibroblasts.

The bradykinin B1-receptor is strongly upregulated under chronic inflammatory conditions. However, the mechanism and reason are not known. Because a better understanding of the mechanism of the upregulation will help in understanding its potential importance in inflammation, we have studied the molecular mechanism of B1-receptor upregulation in cultured human lung fibroblasts (IMR 90) in response to IL-1beta and the B1-agonist [des-Arg10]-kallidin. We show that treatment of human IMR 90 cells by IL-1beta stimulates the expression of both B1-receptor mRNA and protein. The latter was studied by Western blot analysis using antipeptide antibodies directed against the COOH-terminal part of the human B1-receptor. We furthermore report the novel observation that the B1-receptor is upregulated by its own agonist which was completely blocked by the specific B1-antagonist [des-Arg10-Leu9]-kallidin, indicating an upregulation entirely mediated through cell surface B1-receptors. The increased population of B1-receptors was functionally coupled as exemplified by an enhancement of the B1-agonist induced increase in free cytosolic calcium. Upregulation by the B1-agonist was blocked by a specific protein kinase C inhibitor. B1-agonist-induced upregulation was correlated to the induction of transcription factor nuclear factor kappaB (NF-kappaB) which efficiently bound to the NF-kappaB-like sequence located in the promoter region of the human B1-receptor gene. This correlation was further confirmed by reporter gene assays which showed that this NF-kappaB-like sequence, in the B1-receptor promoter context, could contribute to IL-1beta and DLBK-induced B1-receptor transcription activation, and by the effect of NF-kappaB inhibitor pyrrolidinedithiocarbamate which diminished both B1-receptor upregulation and NF-kappaB activation. NF-kappaB is now recognized as a key inflammatory mediator which is activated by the B1-agonist but which is also involved in B1-receptor upregulation