Effet allélopathique de quelques plantes médicinales sur la germination des graines de Phalaris canariensis L. et Lactuca sativa L.

L’utilisation d’un herbicide naturel peut réduire les impacts préjudiciables à l’environnement. Dans ce sens l’allélopathie est considérée comme une technique prometteuse pour la lutte biologique. Cependant, les effets des substances allelopathiques restent peu expérimentés dans les conditions du laboratoire et du champ. Dans cette étude, les extraits aqueux des feuilles de 15 espèces de différentes régions du Maroc ont été testés sur la germination de l’alpiste des canaries (Phalaris canariensis L.) comme plante représentative de la classe des monocotylédones et la laitue (Lactuca sativa L.) représentative des dicotylédones. Il s’est avéré que seules trois espèces sur 15 répondent aux critères d’un herbicide biologique efficace, il s’agit d’Ammi visnaga (L.) Lam., d’Atractylis gummifera L. et de Ruta montana L.. Ainsi, le taux de réduction de la germination de l’alpiste des canaries par ces trois plantes variait entre 96 et 100%, alors que la germination de la laitue n’a pas été affectée et dont le pourcentage d’inhibition était compris entre -8 et 4%. En effet, les extraits aqueux de ces trois plantes ont montré une très bonne efficacité herbicide sur l’alpiste des canaries et peut être la même efficacité sur les monocotylédones et une sélectivité vis-à-vis de la laitue qui serait la même pour les dicotylédones

Role of Interaction and Nucleoside Diphosphate Kinase B in Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator Function by cAMP-Dependent Protein Kinase A

Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-dependent protein kinase A (PKA) and ATP-regulated chloride channel. Here, we demonstrate that nucleoside diphosphate kinase B (NDPK-B, NM23-H2) forms a functional complex with CFTR. In airway epithelia forskolin/IBMX significantly increases NDPK-B co-localisation with CFTR whereas PKA inhibitors attenuate complex formation. Furthermore, an NDPK-B derived peptide (but not its NDPK-A equivalent) disrupts the NDPK-B/CFTR complex in vitro (19-mers comprising amino acids 36-54 from NDPK-B or NDPK-A). Overlay (Far-Western) and Surface Plasmon Resonance (SPR) analysis both demonstrate that NDPK-B binds CFTR within its first nucleotide binding domain (NBD1, CFTR amino acids 351-727). Analysis of chloride currents reflective of CFTR or outwardly rectifying chloride channels (ORCC, DIDS-sensitive) showed that the 19-mer NDPK-B peptide (but not its NDPK-A equivalent) reduced both chloride conductances. Additionally, the NDPK-B (but not NDPK-A) peptide also attenuated acetylcholine-induced intestinal short circuit currents. In silico analysis of the NBD1/NDPK-B complex reveals an extended interaction surface between the two proteins. This binding zone is also target of the 19-mer NDPK-B peptide, thus confirming its capability to disrupt NDPK-B/CFTR complex. We propose that NDPK-B forms part of the complex that controls chloride currents in epithelia

NM23 proteins: innocent bystanders or local energy boosters for CFTR?

NM23 proteins NDPK-A and -B bind to the cystic fibrosis (CF) protein CFTR in different ways from kinases such as PKA, CK2 and AMPK or linkers to cell calcium such as calmodulin and annexins. NDPK-A (not -B) interacts with CFTR through reciprocal AMPK binding/control, whereas NDPK-B (not -A) binds directly to CFTR. NDPK-B can activate G proteins without ligand-receptor coupling, so perhaps NDPK-B's binding influences energy supply local to a nucleotide-binding site (NBD1) needed for CFTR to function. Curiously, CFTR (ABC-C7) is a member of the ATP-binding cassette (ABC) protein family that does not obey 'clan rules'; CFTR channels anions and is not a pump, regulates disparate processes, is itself regulated by multiple means and is so pleiotropic that it acts as a hub that orchestrates calcium signaling through its consorts such as calmodulin/annexins. Furthermore, its multiple partners make CFTR dance to different tunes in different cellular and subcellular locations as it recycles from the plasma membrane to endosomes. CFTR function in airway apical membranes is inhibited by smoking which has been dubbed 'acquired CF'. CFTR alone among family members possesses a trap for other proteins that it unfurls as a 'fish-net' and which bears consensus phosphorylation sites for many protein kinases, with PKA being the most canonical. Recently, the site of CFTR's commonest mutation has been proposed as a knock-in mutant that alters allosteric control of kinase CK2 by log orders of activity towards calmodulin and other substrates after CFTR fragmentation. This link from CK2 to calmodulin that binds the R region invokes molecular paths that control lumen formation, which is incomplete in the tracheas of some CF-affected babies. Thus, we are poised to understand the many roles of NDPK-A and -B in CFTR function and, especially lumen formation, which is defective in the gut and lungs of many CF babies

Effect of ZnO on physical properties of Sb2O3-PbO-ZnO system

International audience— Vitreous systems based on antimony oxide Sb2O3 have been investigated. The limits for glass formation are reported in the Sb2O3-PbO-ZnO ternary system. Thermal measurements implemented by differential scanning calorimetry show that Tg is above 300°C. As a general trend, Tg increases with zinc oxide content. The influence of the ZnO substitution on the optical and physical properties has been studied in the (80−x)Sb2O3-20PbO-xZnO system Vickers micro-hardness, Young’s modulus increase as zinc oxide concentration increases. An inverse dependence is observed for density. U.V. transmission stabilized around 75% and extended IR transmission is obtained. This behavior is discussed in relation to structural hypothesis. © 2019 IEEE