Previous nutritional studies have shown that insulin regulation is different between DT and A strains of gibel carp. As leptin plays a pivotal role in the effects of insulin, we hypothesised that leptin regulation of glucose and lipid metabolism would differ between the two strains. To test our hypothesis, recombinant human leptin was injected into two strains. The results showed that leptin activated the phosphatidylinositol 3-kinase (PI3K)–protein kinase B (AKT), AMP-activated protein kinase–acetyl coenzyme A carboxylase and Janus kinase 2 (JAK2)–signal transducer and activator of transcription (STAT) signalling pathways in both strains. Hypoglycaemia induced by leptin might be due to higher glucose uptake by the liver and muscles together with enhanced glycolytic potential and reduced gluconeogenic potential. Decreased lipogenesis and up-regulated fatty acid oxidation were induced by leptin. In terms of genotype, the PI3K–AKT signalling pathway was more strongly activated by leptin in the muscle tissue of the A strain, as reflected by the heightened phosphorylation of AKT. Furthermore, glycogen content, glycolytic enzyme activity and gluconeogenic capability were higher in the A strain than the DT strain. Strain A had higher levels of fatty acid synthesis and lipolytic capacity in the liver than the DT strain, but the opposite was true in white muscle. Regarding leptin–genotype interactions, the DT strain displayed stronger regulation of glucose metabolism in the liver by leptin as compared with the A strain. Moreover, a more active JAK2–STAT signalling pathway accompanied by enhanced inhibition of fatty acid synthesis by leptin was observed in the DT strain. Overall, the regulation of glucose and lipid metabolism by leptin differed between the two strains, as expected.

Pinoxaden is a POST acetyl coenzyme A carboxylase (ACCase) inhibitor in the phenylpyrazolin chemical family and is labelled for turfgrass use at broadcast rates of 35.5 to 71 g ai ha−1 and spot spray rates of 156 to 310 g ai ha−1. A greenhouse rate-response study was conducted to characterize the efficacy of pinoxaden against common grassy weeds. Weed species examined in this study were yellow foxtail, southern sandbur, annual bluegrass, roughstalk bluegrass, large crabgrass, dallisgrass, bahiagrass, goosegrass, and perennial ryegrass. Nonlinear regressions were modelled to determine visible injury rates (the application rate at which 50% of the weed species were injured and the 90% [I90] rate) and weight reduction rates (the application rate at which there was a 50% reduction in fresh weight and 90% reduction [WR90]) for each weed species. Only annual bluegrass, bahiagrass, and goosegrass had visible injury I90 values greater than the maximum labelled spot spray rate of 310 g ai ha−1. Annual bluegrass, bahiagrass, southern sandbur, and goosegrass all had WR90 values greater than the maximum labelled spot spray rate of 310 g ai ha−1. Results from this study indicate that the evaluated weed species can be ranked, according to visible injury I90 values, from most to least susceptible: perennial ryegrass > yellow foxtail > dallisgrass > large crabgrass > southern sandbur > roughstalk bluegrass > bahiagrass > goosegrass > annual bluegrass.

With the widespread occurrence of herbicide-resistant weeds in midsouthern U.S. rice, new technologies are needed to achieve adequate weed control. A new non–genetically modified rice trait has been commercialized that is resistant to quizalofop, an acetyl coenzyme A carboxylase (ACCase)-inhibiting herbicide. The addition of quizalofop-resistant rice to production systems will increase the use of quizalofop, possibly increasing the risk for injury to other grass crops. Experiments were conducted in 2014 and 2015 to determine the sensitivity of corn, grain sorghum, and conventional rice to low rates of quizalofop (1/10× to 1/200× of 160 g ai ha–1). Conventional rice was not affected by quizalofop rate or application timing. Corn displayed the greatest response to the 1/10× quizalofop rate at the two- to three-leaf stage, with 50% to 65% injury and 35% to 37% relative yield compared to the nontreated check. Grain sorghum was injured 31% to 34% by the 1/10× quizalofop rate applied at the two- to three-leaf stage, and there was 20% to 26% injury at the panicle exertion growth stage. The highest rate of quizalofop at the panicle exertion stage reduced yields 28% to 46%. Overall, risk for injury to any of the three evaluated crops from quizalofop appears low, with greatest injury observed at the highest quizalofop drift rate, with minimal injury at lower rates.

Chlorimuron antagonized the activity of quizalofop on broadleaf signalgrass when applied in greenhouse studies as a postemergence tank mix. In vitro leaf disc assays utilizing 14C-acetate or 14C-pyruvate as substrates were conducted to ascertain the effect of clorimuron and quizalofop on fatty acid biosynthesis and to determine if antagonism between the two herbicides occurs at the biochemical sites of action. Incorporation of 14C-acetate in control treatments was linear with time to 120 min. Acetate incorporation in the presence of quizalofop (1.1 μM) was also linear but was inhibited 30 min after initialization of the reaction. The concentration of quizalofop that inhibited 14C-acetate incorporation 50% (I50) was 0.54 μM. Chlorimuron, up to 155 μM, had no effect on 14C-acetate incorporation. A mixture of quizalofop (1.1 μM) and chlorimuron (4.8 μM) inhibited 14C-acetate incorporation similar to that of quizalofop alone at 1.1 μM. Quizalofop I50 for incorporation of 14C-pyruvate was 1.1 μM, and clorimuron at 4.8 μM decreased incorporation 15%. Excess unlabeled pyruvate (5 μM) had no effect on either 14C-acetate or 14C-pyruvate incorporation in the presence of both herbicides. It is believed that antagonism of quizalofop by clorimuron is not due to an excess pool of pyruvate resulting from inhibition of acetolactate synthase by chlorimuron.

The herbicide pinoxaden is a phenylpyrazoline inhibitor of acetyl coenzyme A carboxylase. Research was conducted to determine the effects of pinoxaden (90 g ai ha−1) alone and in combination with herbicide safeners on creeping bentgrass injury as well as perennial ryegrass and roughstalk bluegrass control. Greenhouse experiments determined that herbicide safeners cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl were more effective in reducing creeping bentgrass injury from pinoxaden than benoxacor, isoxadifen-ethyl, and naphthalic-anhydride. Other experiments determined that creeping bentgrass injury from pinoxaden decreased as rates (0, 23, 45, 68, 90, 225, or 450 g ha−1) of cloquintocet-mexyl, fenchlorazole-ethyl, and mefenpyr-diethyl increased. On the basis of creeping bentgrass responses to various safener rates, safeners were applied at 68 and 450 g ha−1 in additional experiments to evaluate their effects on pinoxaden (90 g ha−1) injury to creeping bentgrass and efficacy against perennial ryegrass and roughstalk bluegrass. In these experiments, safeners mefenpyr-diethyl and cloquintocet-mexyl reduced pinoxaden-induced creeping bentgrass injury (from 25 to ≤ 5%) more than fenchlorazole-ethyl at 2 wk after treatment. Safeners reduced pinoxaden efficacy against roughstalk bluegrass. Perennial ryegrass was controlled > 80% by pinoxaden and herbicide safeners did not reduce control. Field experiments should evaluate pinoxaden in combination with cloquintocet-mexyl and mefenpyr-diethyl to optimize safener : herbicide ratios and rates for creeping bentgrass safety as well as perennial ryegrass and roughtstalk bluegrass control in different climates and seasons.

A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P-ethyl. An 11-fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha–1) with susceptible plants (20 g ae ha–1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim at the field rate. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P-ethyl, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P-ethyl resistance in this population is due to a non–target-site mechanism or mechanisms.

Surviving rigid ryegrass plants were collected from a cropping field at Pindar, Western Australia (population WALR 50), after inadequate control by glyphosate applied at the normal field rate. Plants were grown to maturity in pots and seeds were collected. Glyphosate dose–response experiments with known susceptible and resistant control populations confirmed the resistant status of the WALR 50 population. The glyphosate rate resulting in 5% mortality (LD50) and GR50 (the glyphosate rate required to reduce mean growth of individuals to 50% of the untreated control) values for this population were 1,069 and 217 g ae ha−1, respectively, corresponding to R:S ratios of 3.4 and 1.9 for mortality and growth. In addition, a novel root growth–based assay of glyphosate resistance was developed and validated, giving a root growth GR50 R:S ratio of 3.4. A resistance profile was established by assessing population-level survival of WALR 50 after applications at recommended rates of a range of herbicides commonly used for rigid ryegrass control in Australia. High levels of resistance to the acetolactate synthase (ALS)–inhibiting sulfonylurea herbicides chlorsulfuron and sulfometuron, moderate resistance to the acetyl coenzyme A carboxylase (ACCase)–inhibiting herbicide diclofop, and low levels of resistance to the imidazilinone herbicide imazethapyr were found. More detailed dose–response experiments confirmed resistance to chlorsulfuron, sulfometuron, and diclofop. In vitro enzyme-inhibition studies demonstrated that ALS resistance in WALR 50 is due to an insensitive target enzyme and that ACCase resistance is due to a nontarget site–based mechanism. WALR 50 is the first glyphosate-resistant weed population with confirmed resistance to ACCase- and ALS-inhibiting herbicides.