Aerobic C–H Acetoxylation of 8‑Methylquinoline in Pd^II–Pyridinecarboxylic Acid Systems: Some Structure–Reactivity Relationships

Catalytic oxidative C–H acetoxylation of 8-methylquinoline as a model substrate with O₂ as oxidant was performed using palladium­(II) carboxylate catalysts derived from four different pyridinecarboxylic acids able to form palladium­(II) chelates of different size. A comparison of the rates of the substrate C–H activation and the O₂ activation steps shows that the C–H activation step is rate-limiting, whereas the O₂ activation occurs at a much faster rate already at 20 °C. The chelate ring size and the chelate ring strain of the catalytically active species are proposed to be the key factors affecting the rate of the C–H activation

Aerobic C–H Acetoxylation of 8‑Methylquinoline in Pd^II–Pyridinecarboxylic Acid Systems: Some Structure–Reactivity Relationships

Catalytic oxidative C–H acetoxylation of 8-methylquinoline as a model substrate with O₂ as oxidant was performed using palladium­(II) carboxylate catalysts derived from four different pyridinecarboxylic acids able to form palladium­(II) chelates of different size. A comparison of the rates of the substrate C–H activation and the O₂ activation steps shows that the C–H activation step is rate-limiting, whereas the O₂ activation occurs at a much faster rate already at 20 °C. The chelate ring size and the chelate ring strain of the catalytically active species are proposed to be the key factors affecting the rate of the C–H activation

Dopamine Receptors Antagonistically Regulate Behavioral Choice between Conflicting Alternatives in <i>C. elegans</i>

<div><p><i>Caenorhabditis elegans</i> is a useful model to study the neuronal or molecular basis for behavioral choice, a specific form of decision-making. Although it has been implied that both D1-like and D2-like dopamine receptors may contribute to the control of decision-making in mammals, the genetic interactions between D1-like and D2-like dopamine receptors in regulating decision-making are still largely unclear. In the present study, we investigated the molecular control of behavioral choice between conflicting alternatives (diacetyl and Cu²⁺) by D1-like and D2-like dopamine receptors and their possible genetic interactions with <i>C. elegans</i> as the assay system. In the behavioral choice assay system, mutation of <i>dop-1</i> gene encoding D1-like dopamine receptor resulted in the enhanced tendency to cross the Cu²⁺ barrier compared with wild-type. In contrast, mutations of <i>dop-2</i> or <i>dop-3</i> gene encoding D2-like dopamine receptor caused the weak tendency to cross the Cu²⁺ barrier compared with wild-type. During the control of behavioral choice, DOP-3 antagonistically regulated the function of DOP-1. The behavioral choice phenotype of <i>dop-2; dop-1dop-3</i> triple mutant further confirmed the possible antagonistic function of D2-like dopamine receptor on D1-like dopamine receptor in regulating behavioral choice. The genetic assays further demonstrate that DOP-3 might act through Gα_o signaling pathway encoded by GOA-1 and EGL-10, and DOP-1 might act through Gα_q signaling pathway encoded by EGL-30 and EAT-16 to regulate the behavioral choice. DOP-1 might function in cholinergic neurons to regulate the behavioral choice, whereas DOP-3 might function in GABAergic neurons, RIC, and SIA neurons to regulate the behavioral choice. In this study, we provide the genetic evidence to indicate the antagonistic relationship between D1-like dopamine receptor and D2-like dopamine receptor in regulating the decision-making of animals. Our data will be useful for understanding the complex functions of dopamine receptors in regulating decision-making in animals.</p></div

Effects of D1-like dopamine receptor on behavioral choice between conflicting alternatives.

<p>(A) Assay model for the behavioral choice between conflicting alternatives. (B) Phenotypes of <i>dop-1</i> and <i>dop-4</i> mutants in the interaction assay under the well-fed or starved condition. In the assay system, the Cu²⁺ ion concentration was 100 mM, and the diacetyl concentration was 10⁻². (C) Dose-response curves of wild-type N2 and <i>dop-1</i> mutants to diacetyl with (+) or without (-) 100 mM of Cu²⁺ ion. Differences between groups were determined using two-way ANOVA. (D) Dose-response curves of wild-type N2 and <i>dop-1</i> mutants to Cu²⁺ ion with (+) or without (-) 10⁻² of diacetyl. Differences between groups were determined using two-way ANOVA. (E) Locomotion behavior of wild-type N2 and <i>dop-1</i> mutants in the absence (-) of food under well-fed or starved condition. Locomotion behavior was assessed by the body bend. Bars represent mean ± S.E.M. **<i>P</i> <0.01 <i>vs</i> N2 (if not specially indicated).</p

Neuron-specific activity of DOP-1 or DOP-3 in regulating behavioral choice.

<p>(A) Neuron-specific activity of DOP-1 in regulating behavioral choice. (B) Neuron-specific activity of DOP-3 in regulating behavioral choice. The behavioral choice was examined under the well-fed condition. In the assay system, the Cu²⁺ ion concentration was 100 mM, and the diacetyl concentration was 10⁻². In the rescue experiments, <i>hlh-17</i> promoter was used for glia-specific expression, <i>unc-47</i> promoter was used for GABAergic neurons-specific expression, <i>acr-2</i> promoter was used for cholinergic neuron-specific expression, <i>gcy-28.d</i> promoter was used for AIA-specific expression, <i>ttx-3</i> promoter was used for AIY-specific expression, <i>tbh-1</i> promoter was used for RIC-specific expression, <i>gcy-7</i> promoter was used for ASE-specific expression, <i>sro-1</i> promoter was used for expression in SIA neurons, and <i>lim-6</i> promoter was used for expression in RIS neurons. Bars represent mean ± S.E.M. **<i>P</i><0.01.</p

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Response of <i>let-7</i> to <i>P</i>. <i>aeruginosa</i> PA14 infection.

<p>(A) Effect of <i>P</i>. <i>aeruginosa</i> PA14 infection on <i>let-7</i>::<i>GFP</i> expression. Arrowheads indicate the neurons. Pharynx (*) and intestine (**) were also indicated. Nematodes were infected with <i>P</i>. <i>aeruginosa</i> PA14 for 24-h. Thirty animals were examined. Bars represent mean ± SD. **<i>P</i> < 0.01 <i>vs</i> OP50. (B) Comparison of <i>P</i>. <i>aeruginosa</i> PA14 CFU between wild-type N2 and <i>let-7(mg279)</i> mutants infected with <i>P</i>. <i>aeruginosa</i> PA14. Bars represent mean ± SD. **<i>P</i> < 0.01 <i>vs</i> wild-type. (C) Quantitative real-time PCR analysis of expression patterns of the anti-microbial peptide genes in <i>let-7(mg279)</i> mutant infected with <i>P</i>. <i>aeruginosa</i> PA14. Normalized expression is presented relative to wild-type expression. Bars represent mean ± SD.</p

Roles of Gα_q signaling pathway in regulating behavioral choice between conflicting alternatives.

<p>(A) Phenotypes of Gα_q signaling pathway mutants in the interaction assay under the well-fed or starved condition. In the assay system, the Cu²⁺ ion concentration was 100 mM, and the diacetyl concentration was 10⁻². (B) Dose-response curves of wild-type N2 and mutants to diacetyl with (+) or without (-) 100 mM of Cu²⁺ ion. Differences between groups were determined using two-way ANOVA. (C) Dose-response curves of wild-type N2 and mutants to Cu²⁺ ion with (+) or without (-) 10⁻² of diacetyl. Differences between groups were determined using two-way ANOVA. (D) Locomotion behavior of wild-type N2 and mutants in the absence (-) of food under the well-fed or starved condition. Locomotion behavior was assessed by the body bend. Bars represent mean ± S.E.M. **<i>P</i><0.01 <i>vs</i> N2 (if not specially indicated).</p

Genetic interactions between SDZ-24 and some known signaling pathways in the regulation of innate immune response to <i>P</i>. <i>aeruginosa</i> PA14 infection.

<p>(A) Genetic interaction between SDZ-24 and PMK-1, DAF-16, or DBL-1 in the regulation of survival in <i>P</i>. <i>aeruginosa</i> PA14 infected nematodes. Statistical comparisons of the survival plots indicate that, after <i>P</i>. <i>aeruginosa</i> PA14 infection, the survival of <i>Ex(</i>P<i>ges-1-sdz-24);pmk-1(RNAi)</i> (<i>P</i> < 0.0001) was significantly different from that of <i>Ex(</i>P<i>ges-1-sdz-24)</i>, and the survival of <i>daf-16(RNAi);Ex(</i>P<i>ges-1-sdz-24)</i> (<i>P</i> = 0.9463) or <i>Ex(</i>P<i>ges-1-sdz-24);dbl-1(RNAi)</i> (<i>P</i> = 0.9619) was not significantly different from that of <i>Ex(</i>P<i>ges-1-sdz-24)</i>. (B) Genetic interaction between SDZ-24 and PMK-1, SEK-1, or NSY-1 in the regulation of survival in <i>P</i>. <i>aeruginosa</i> PA14 infected nematodes. Statistical comparisons of the survival plots indicate that, after <i>P</i>. <i>aeruginosa</i> PA14 infection, the survival of <i>Ex(</i>P<i>ges-1-sdz-24);pmk-1(RNAi)</i>, <i>Ex(</i>P<i>ges-1-sdz-24);sek-1(RNAi)</i>, or <i>Ex(</i>P<i>ges-1-sdz-24);nsy-1(RNAi)</i> was significantly different from that of <i>Ex(</i>P<i>ges-1-sdz-24)</i> (<i>P</i> < 0.0001). (C) Genetic interaction between SDZ-24 and PMK-1, SEK-1, or NSY-1 in the regulation of CFU of <i>P</i>. <i>aeruginosa</i> PA14 in <i>P</i>. <i>aeruginosa</i> PA14 infected nematodes. (D) Genetic interaction between SDZ-24 and PMK-1, SEK-1, or NSY-1 in the regulation of expression patterns of anti-microbial genes in <i>P</i>. <i>aeruginosa</i> PA14 infected nematodes. Normalized expression is presented relative to wild-type expression. Bars represent mean ± SD. **<i>P</i> < 0.01 <i>vs</i> wild-type (if not specially indicated).</p

Model for dopamine receptors in regulating behavioral choice between conflicting alternatives in nematodes.

<p>Model for dopamine receptors in regulating behavioral choice between conflicting alternatives in nematodes.</p