Vertical intertidal variation of organic matter stocks and patterns of sediment deposition in a mesotidal coastal wetland

Tidal coastal wetlands, common home to seagrass and salt marshes, are relevant carbon sinks due to their high capacity to accumulate and store organic carbon in their sediments. Recent studies demonstrated that the spatial variability of this organic carbon within the same wetland system can be significant. Some of the environmental drivers of this spatial variability remain understudied and the selection of the most relevant ones can be context dependent. Here we investigated the role of bed elevation, hydrodynamics, and habitat type (salt marsh and seagrass) on the organic matter (OM) net deposition-resuspension rate and superficial sedimentary stocks (top 5 cm) at the tidal wetlands of the Ria Formosa, a mesotidal coastal lagoon in South Portugal. Results showed that two vectors of spatial variation need to be considered to describe the intertidal sedimentary OM stocks: the bed elevation that imposes a decrease of the hydroperiod and thus the change of habitat from the lower seagrass Z. noltei to the upper saltmarsh S. maritimus, and the horizontal spatial variation along the secondary channels of the lagoon that imposes a decrease in the current flow velocity magnitude. The multiple linear regression analyses, using data from 40 sampling points, explained 59% of the variation of the superficial sedimentary stocks of OM in salt marshes and seagrasses of the Ria Formosa lagoon and revealed that stocks generally decrease with elevation, yet with variation among sites and habitats. It was also found that the decrease of the OM net deposition-resuspension rate with bed elevation was exponential. Our study emphasizes the importance of considering multiple environmental drivers and spatial variation for regional estimations of organic matter (and organic carbon) sedimentary stocks in coastal wetlands.info:eu-repo/semantics/publishedVersio

Persistent cAMP-Signals Triggered by Internalized G-Protein–Coupled Receptors

Real-time monitoring of G-protein-coupled receptor (GPCR) signaling in native cells suggests that the receptor for thyroid stimulating hormone remains active after internalization, challenging the current model for GPCR signaling

Signalisation mitochondriale des récepteurs couplés aux protéines G

Les récepteurs couplés aux protéines G (RCPG) forment la plus grande famille de récepteurs membranaires avec 800 membres chez l’Homme qui sont exprimés à la surface de la cellule où ils répondent à un large panel de stimuli extracellulaires. Des avancées récentes indiquent que les RCPG sont également exprimés dans des compartiments intracellulaires où ils remplissent des fonctions importantes. Dans cette revue, nous nous intéresserons à la localisation et à la fonction des RCPG exprimés dans les mitochondries

Involvement of STAT5 (signal transducer and activator of transcription 5) and HNF-4 (hepatocyte nuclear factor 4) in the transcriptional control of the hnf6 gene by growth hormone

HNF-6 is a tissue-restricted transcription factor that participates in the regulation of several genes in liver. We reported earlier that in adult rats, HNF-6 mRNA concentration in liver drops to almost undetectable levels after hypophysectomy and returns to normal after 1 week of GH treatment. We now show that this results from a rapid effect of GH, and we characterize its molecular mechanism. In hypophysectomized rats, HNF-6 mRNAs increased within 1 h after a single injection of GH. The same GH-dependent induction was reproduced on isolated hepatocytes. To determine whether GH regulates hnf6 expression at the gene level, we studied its promoter. DNA binding experiments showed that 1) the transcription factors STAT5 (signal transducer and activator of transcription 5) and HNF-4 (hepatocyte nuclear factor 4) bind to sites located around -110 and -650, respectively; and 2) STAT5 binding is induced and HNF-4 binding affinity is increased in liver within 1 h after GH injection to hypophysectomized rats. Using transfection experiments and site-directed mutagenesis, we found that STAT5 and HNF-4 stimulated transcription of an hnf6 gene promoter-reporter construct. Furthermore, GH stimulated transcription of this construct in cells that express GH receptors. Consistent with our earlier finding that HNF-6 stimulates the hnf4 and hnf3beta gene promoters, GH treatment of hypophysectomized rats increased the liver concentration of HNF-4 and HNF-3beta mRNAs. Together, these data demonstrate that GH stimulates transcription of the hnf6 gene by a mechanism involving STAT5 and HNF-4. They show that HNF-6 participates not only as an effector, but also as a target, to the regulatory network of liver transcription factors, and that several members of this network are GH regulated