The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
David G. Barker - One of the best experts on this subject based on the ideXlab platform.
-
Rhizobium Nod Factor Signaling: Evidence for a G Protein–Mediated Transduction Mechanism
The Plant Cell, 1998Co-Authors: Jean-luc Pingret, Etienne-pascal Journet, David G. BarkerAbstract:Rhizobium nodulation (Nod) factors are lipochitooligosaccharide signals that elicit key symbiotic developmental responses in the host legume root. In this study, we have investigated Nod factor signal Transduction in the Medicago root epidermis by using a pharmacological approach in conjunction with transgenic plants expressing the Nod factor–responsive reporter construct pMtENOD12–GUS . Evidence for the participation of heterotrimeric G proteins in Nod factor signaling has come from three complementary observations: (1) the amphiphilic peptides mastoparan and Mas7, known G protein agonists, are able to mimic Nod factor–induced epidermal MtENOD12 expression; (2) growth of plants in nodulation-inhibiting conditions (10 mM NH 4 NO 3 ) leads to a dramatic reduction in both Nod factor– and mastoparan-elicited gene expression; and (3) bacterial pertussis toxin, a well-characterized G protein antagonist, blocks the activities of both the Nod factor and mastoparan. In addition, we have found that antagonists that interfere with phospholipase C activity (neomycin and U73122) and Ca 2+ influx/release (EGTA, La 3+ , and ruthenium red) block Nod factor/mastoparan activity. Taken together, these results are consistent with a Nod factor signal Transduction Mechanism involving G protein mediation coupled to the activation of both phosphoinositide and Ca 2+ second messenger pathways.
-
rhizobium nod factor signaling evidence for a g protein mediated Transduction Mechanism
The Plant Cell, 1998Co-Authors: Jean-luc Pingret, Etienne-pascal Journet, David G. BarkerAbstract:Rhizobium nodulation (Nod) factors are lipochitooligosaccharide signals that elicit key symbiotic developmental responses in the host legume root. In this study, we have investigated Nod factor signal Transduction in the Medicago root epidermis by using a pharmacological approach in conjunction with transgenic plants expressing the Nod factor–responsive reporter construct pMtENOD12–GUS . Evidence for the participation of heterotrimeric G proteins in Nod factor signaling has come from three complementary observations: (1) the amphiphilic peptides mastoparan and Mas7, known G protein agonists, are able to mimic Nod factor–induced epidermal MtENOD12 expression; (2) growth of plants in nodulation-inhibiting conditions (10 mM NH 4 NO 3 ) leads to a dramatic reduction in both Nod factor– and mastoparan-elicited gene expression; and (3) bacterial pertussis toxin, a well-characterized G protein antagonist, blocks the activities of both the Nod factor and mastoparan. In addition, we have found that antagonists that interfere with phospholipase C activity (neomycin and U73122) and Ca 2+ influx/release (EGTA, La 3+ , and ruthenium red) block Nod factor/mastoparan activity. Taken together, these results are consistent with a Nod factor signal Transduction Mechanism involving G protein mediation coupled to the activation of both phosphoinositide and Ca 2+ second messenger pathways.
Anna Maria Liscia - One of the best experts on this subject based on the ideXlab platform.
-
Transduction Mechanism(s) of Na-saccharin in the blowfly Protophormia terraenovae: evidence for potassium and calcium conductance involvement.
Journal of comparative physiology. A Neuroethology sensory neural and behavioral physiology, 2009Co-Authors: Carla Masala, Paolo Solari, Giorgia Sollai, Roberto Massimo Crnjar, Anna Maria LisciaAbstract:The study on Transduction Mechanisms underlying bitter stimuli is a particularly intriguing challenge for taste researchers. The present study investigates, in the labellar chemosensilla of the blowfly Protophormia terraenovae, the Transduction Mechanism by which saccharin evokes the response of the "deterrent" cell, with particular attention to the contribution of K(+) and Ca(2+) current and the role of cyclic nucleotides, since second messengers modulate Ca(2+), Cl(-) and K(+) currents to different extents. As assessed by extracellular single-sensillum recordings, our results show that the addition of a Ca(2+) chelator such as EGTA or the Ca(2+) current blockers SK&F-96365, Mibefradil, Nifedipine and W-7 decrease the response of the "deterrent" cell to saccharin. A similar decreasing effect was also obtained following the addition of 4-aminopyridine, a K(+) current blocker. On the contrary, the membrane-permeable cyclic nucleotide 8-bromoguanosine 3',5'-cyclic monophosphate (8Br-cGMP) activates this cell and shows an additive effect when presented mixed with saccharin. Our results are consistent with the hypothesis that in the labellar chemosensilla of the blowfly both Ca(2+) and K(+) ions are involved in the Transduction Mechanism of the "deterrent" cell in response to saccharin. Our results also suggest a possible pathway common to saccharin and 8Br-cGMP.
-
Transduction Mechanism(s) of Na-saccharin in the blowfly Protophormia terraenovae: evidence for potassium and calcium conductance involvement A Neuroethology, sensory, neural, and behavioral physiology
Journal of Comparative Physiology A-neuroethology Sensory Neural and Behavioral Physiology, 2009Co-Authors: Carla Masala, Paolo Solari, Giorgia Sollai, Roberto Massimo Crnjar, Anna Maria LisciaAbstract:The study on Transduction Mechanisms underlying bitter stimuli is a particularly intriguing challenge for taste researchers. The present study investigates, in the labellar chemosensilla of the blowfly Protophormia terraenovae, the Transduction Mechanism by which saccharin evokes the response of the “deterrent” cell, with particular attention to the contribution of K⁺ and Ca²⁺ current and the role of cyclic nucleotides, since second messengers modulate Ca²⁺, Cl⁻ and K⁺ currents to different extents. As assessed by extracellular single-sensillum recordings, our results show that the addition of a Ca²⁺ chelator such as EGTA or the Ca²⁺ current blockers SK&F-96365, Mibefradil, Nifedipine and W-7 decrease the response of the “deterrent” cell to saccharin. A similar decreasing effect was also obtained following the addition of 4-aminopyridine, a K⁺ current blocker. On the contrary, the membrane-permeable cyclic nucleotide 8-bromoguanosine 3′,5′-cyclic monophosphate (8Br-cGMP) activates this cell and shows an additive effect when presented mixed with saccharin. Our results are consistent with the hypothesis that in the labellar chemosensilla of the blowfly both Ca²⁺ and K⁺ ions are involved in the Transduction Mechanism of the “deterrent” cell in response to saccharin. Our results also suggest a possible pathway common to saccharin and 8Br-cGMP.
Jean-luc Pingret - One of the best experts on this subject based on the ideXlab platform.
-
Rhizobium Nod Factor Signaling: Evidence for a G Protein–Mediated Transduction Mechanism
The Plant Cell, 1998Co-Authors: Jean-luc Pingret, Etienne-pascal Journet, David G. BarkerAbstract:Rhizobium nodulation (Nod) factors are lipochitooligosaccharide signals that elicit key symbiotic developmental responses in the host legume root. In this study, we have investigated Nod factor signal Transduction in the Medicago root epidermis by using a pharmacological approach in conjunction with transgenic plants expressing the Nod factor–responsive reporter construct pMtENOD12–GUS . Evidence for the participation of heterotrimeric G proteins in Nod factor signaling has come from three complementary observations: (1) the amphiphilic peptides mastoparan and Mas7, known G protein agonists, are able to mimic Nod factor–induced epidermal MtENOD12 expression; (2) growth of plants in nodulation-inhibiting conditions (10 mM NH 4 NO 3 ) leads to a dramatic reduction in both Nod factor– and mastoparan-elicited gene expression; and (3) bacterial pertussis toxin, a well-characterized G protein antagonist, blocks the activities of both the Nod factor and mastoparan. In addition, we have found that antagonists that interfere with phospholipase C activity (neomycin and U73122) and Ca 2+ influx/release (EGTA, La 3+ , and ruthenium red) block Nod factor/mastoparan activity. Taken together, these results are consistent with a Nod factor signal Transduction Mechanism involving G protein mediation coupled to the activation of both phosphoinositide and Ca 2+ second messenger pathways.
-
rhizobium nod factor signaling evidence for a g protein mediated Transduction Mechanism
The Plant Cell, 1998Co-Authors: Jean-luc Pingret, Etienne-pascal Journet, David G. BarkerAbstract:Rhizobium nodulation (Nod) factors are lipochitooligosaccharide signals that elicit key symbiotic developmental responses in the host legume root. In this study, we have investigated Nod factor signal Transduction in the Medicago root epidermis by using a pharmacological approach in conjunction with transgenic plants expressing the Nod factor–responsive reporter construct pMtENOD12–GUS . Evidence for the participation of heterotrimeric G proteins in Nod factor signaling has come from three complementary observations: (1) the amphiphilic peptides mastoparan and Mas7, known G protein agonists, are able to mimic Nod factor–induced epidermal MtENOD12 expression; (2) growth of plants in nodulation-inhibiting conditions (10 mM NH 4 NO 3 ) leads to a dramatic reduction in both Nod factor– and mastoparan-elicited gene expression; and (3) bacterial pertussis toxin, a well-characterized G protein antagonist, blocks the activities of both the Nod factor and mastoparan. In addition, we have found that antagonists that interfere with phospholipase C activity (neomycin and U73122) and Ca 2+ influx/release (EGTA, La 3+ , and ruthenium red) block Nod factor/mastoparan activity. Taken together, these results are consistent with a Nod factor signal Transduction Mechanism involving G protein mediation coupled to the activation of both phosphoinositide and Ca 2+ second messenger pathways.
Ping Wang - One of the best experts on this subject based on the ideXlab platform.
-
A novel experimental research based on taste cell chips for taste Transduction Mechanism
Sensors and Actuators B: Chemical, 2008Co-Authors: Wei Zhang, Qingjun Liu, Hua Cai, Ping WangAbstract:Abstract Recent advantages in electrophysiological technique on detecting potential and ion changes of taste cells make great progress in developing taste Transduction Mechanisms of taste receptor cells (TRCs). Light-addressable potentiometric sensor (LAPS) is used to detect extracellular potential of TRCs cultured on the silicon chip and to test the taste cell response to taste stimuli of NaCl, HCl, MgSO 4 , sucrose and glumate. Results show that the system composed of LAPS and TRCs is sensitive to gustatorius changes, which has great potential to monitor electrophysiology property of living TRCs. It is a novel non-invasive method to study taste Transduction Mechanisms in vitro for a long term.
Carla Masala - One of the best experts on this subject based on the ideXlab platform.
-
Transduction Mechanism(s) of Na-saccharin in the blowfly Protophormia terraenovae: evidence for potassium and calcium conductance involvement.
Journal of comparative physiology. A Neuroethology sensory neural and behavioral physiology, 2009Co-Authors: Carla Masala, Paolo Solari, Giorgia Sollai, Roberto Massimo Crnjar, Anna Maria LisciaAbstract:The study on Transduction Mechanisms underlying bitter stimuli is a particularly intriguing challenge for taste researchers. The present study investigates, in the labellar chemosensilla of the blowfly Protophormia terraenovae, the Transduction Mechanism by which saccharin evokes the response of the "deterrent" cell, with particular attention to the contribution of K(+) and Ca(2+) current and the role of cyclic nucleotides, since second messengers modulate Ca(2+), Cl(-) and K(+) currents to different extents. As assessed by extracellular single-sensillum recordings, our results show that the addition of a Ca(2+) chelator such as EGTA or the Ca(2+) current blockers SK&F-96365, Mibefradil, Nifedipine and W-7 decrease the response of the "deterrent" cell to saccharin. A similar decreasing effect was also obtained following the addition of 4-aminopyridine, a K(+) current blocker. On the contrary, the membrane-permeable cyclic nucleotide 8-bromoguanosine 3',5'-cyclic monophosphate (8Br-cGMP) activates this cell and shows an additive effect when presented mixed with saccharin. Our results are consistent with the hypothesis that in the labellar chemosensilla of the blowfly both Ca(2+) and K(+) ions are involved in the Transduction Mechanism of the "deterrent" cell in response to saccharin. Our results also suggest a possible pathway common to saccharin and 8Br-cGMP.
-
Transduction Mechanism(s) of Na-saccharin in the blowfly Protophormia terraenovae: evidence for potassium and calcium conductance involvement A Neuroethology, sensory, neural, and behavioral physiology
Journal of Comparative Physiology A-neuroethology Sensory Neural and Behavioral Physiology, 2009Co-Authors: Carla Masala, Paolo Solari, Giorgia Sollai, Roberto Massimo Crnjar, Anna Maria LisciaAbstract:The study on Transduction Mechanisms underlying bitter stimuli is a particularly intriguing challenge for taste researchers. The present study investigates, in the labellar chemosensilla of the blowfly Protophormia terraenovae, the Transduction Mechanism by which saccharin evokes the response of the “deterrent” cell, with particular attention to the contribution of K⁺ and Ca²⁺ current and the role of cyclic nucleotides, since second messengers modulate Ca²⁺, Cl⁻ and K⁺ currents to different extents. As assessed by extracellular single-sensillum recordings, our results show that the addition of a Ca²⁺ chelator such as EGTA or the Ca²⁺ current blockers SK&F-96365, Mibefradil, Nifedipine and W-7 decrease the response of the “deterrent” cell to saccharin. A similar decreasing effect was also obtained following the addition of 4-aminopyridine, a K⁺ current blocker. On the contrary, the membrane-permeable cyclic nucleotide 8-bromoguanosine 3′,5′-cyclic monophosphate (8Br-cGMP) activates this cell and shows an additive effect when presented mixed with saccharin. Our results are consistent with the hypothesis that in the labellar chemosensilla of the blowfly both Ca²⁺ and K⁺ ions are involved in the Transduction Mechanism of the “deterrent” cell in response to saccharin. Our results also suggest a possible pathway common to saccharin and 8Br-cGMP.
