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Diamide insecticide resistance in transgenic Drosophila and Sf9-cells expressing a full-length diamondback moth ryanodine receptor carrying an I4790M mutation.
Pest Manag Sci
March 2022
Department of Biointeractions and Crop Protection, Rothamsted Research, Harpenden, UK.
Background: Resistance to diamide insecticides in Lepidoptera is known to be caused primarily by amino acid changes on the ryanodine receptor (RyR). Recently, two new target site mutations, G4946V and I4790M, have emerged in populations of diamondback moth, Plutella xylostella, as well as in other lepidopteran species, and both mutations have been shown empirically to decrease diamide efficacy. Here, we quantify the impact of the I4790M mutation on diamide activation of the receptor, as compared to alterations at the G4946 locus.
View Article and Find Full Text PDFExpression of mutant huntingtin in leptin receptor-expressing neurons does not control the metabolic and psychiatric phenotype of the BACHD mouse.
PLoS One
June 2013
Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Metabolic and psychiatric disturbances occur early on in the clinical manifestation of Huntington's disease (HD), a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. Hypothalamus has emerged as an important site of pathology and alterations in this area and its neuroendocrine circuits may play a role in causing early non-motor symptoms and signs in HD. Leptin is a hormone that controls energy homeostasis by signaling through leptin receptors in the hypothalamus.
View Article and Find Full Text PDFBrief dopaminergic stimulations produce transient physiological changes in prefrontal pyramidal neurons.
Brain Res
January 2011
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA.
In response to food reward and other pertinent events, midbrain dopaminergic neurons fire short bursts of action potentials causing a phasic release of dopamine in the prefrontal cortex (rapid and transient increases in cortical dopamine concentration). Here we apply short (2s) iontophoretic pulses of glutamate, GABA, dopamine and dopaminergic agonists locally, onto layer 5 pyramidal neurons in brain slices of the rat medial prefrontal cortex (PFC). Unlike glutamate and GABA, brief dopaminergic pulses had negligible effects on the resting membrane potential.
View Article and Find Full Text PDFCrystal structure of hormone-bound atrial natriuretic peptide receptor extracellular domain: rotation mechanism for transmembrane signal transduction.
J Biol Chem
July 2004
Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
A cardiac hormone, atrial natriuretic peptide (ANP), plays a major role in blood pressure and volume regulation. ANP activities are mediated by a single span transmembrane receptor carrying intrinsic guanylate cyclase activity. ANP binding to its extracellular domain stimulates guanylate cyclase activity by an as yet unknown mechanism.
View Article and Find Full Text PDFMutations in the extracellular amino-terminal domain of the NK2 neurokinin receptor abolish cAMP signaling but preserve intracellular calcium responses.
J Biol Chem
November 2002
CNRS UPR9050, Récepteurs et Protéines Membranaires, Ecole Supérieure de Biotechnologie de Strasbourg, Boulevard Sébastien Brandt, Illkirch 67400, France.
By combining real time measurements of agonist binding, by fluorescence resonance energy transfer, and of subsequent responses, we proposed previously that the neurokinin NK2 receptor preexists in equilibrium between three states: inactive, calcium-triggering, and cAMP-producing. Thr(24) and Phe(26) of the NK2 receptor extracellular domain are considered to interact with neuropeptide agonists based on the reduction of affinity when they are substituted by alanine. Using fluorescence resonance energy transfer, we now quantify the binding kinetics of two Texas Red-modified neurokinin A agonists to the fluorescent wild-type (Y-NK2wt) and the mutant (Y-NK2mut) receptor carrying Thr(24) --> Ala and Phe(26) --> Ala mutations.
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