Patients with type 2 diabetes have increased risks for dyslipidaemia and subsequently for developing vascular complications. A recent meta-analysis found that cetoleic acid (C22:1n-11) rich fish oils resulted in lower cholesterol concentration in rodents. The aim was to investigate the effect of consuming fish oils with or without cetoleic acid on serum cholesterol concentration in diabetic rats and to elucidate any effects on cholesterol metabolism. Eighteen male Zucker Diabetic Sprague Dawley rats were fed diets containing herring oil (HERO) or anchovy oil (ANCO) or a control diet with soyabean oil for 5 weeks. The HERO diet contained 0·70 % cetoleic acid, with no cetoleic acid in the ANCO diet. The HERO and ANCO diets contained 0·35 and 0·37 wt% EPA + DHA, respectively. Data were analysed using one-way ANOVA. The serum total cholesterol concentration was 14 % lower in the HERO group compared with ANCO and Control groups (P = 0·023). The HERO group had a higher faecal excretion of bile acids (P = 0·0036), but the cholesterol production in the liver, the hepatic secretion of VLDL and the liver’s capacity to take up cholesterol were similar to controls. The ANCO diet did not affect the serum cholesterol concentration, but the hepatic cholesterol biosynthesis, the clearance of lipoprotein cholesterol and the excretion of bile acids in faeces were higher than in the Control group. To conclude, consumption of herring oil, but not of anchovy oil, led to a lower cholesterol concentration in a type 2 diabetes rat model.

Protoporphyrinogen oxidase (PPO)-inhibiting herbicides remain an important and useful chemistry 60 yr after their first introduction. In this review, based on topics introduced at the Weed Science Society of America 2021 symposium titled “A History, Overview, and Plan of Action on PPO Inhibiting Herbicides,” we discuss the current state of PPO-inhibiting herbicides. Renewed interest in the PPO-inhibiting herbicides in recent years, due to increased use and increased cases of resistance, has led to refinements in knowledge regarding the mechanism of action of PPO inhibitors. Herein we discuss the importance of the two isoforms of PPO in plants, compile a current knowledge of target-site resistance mechanisms, examine non–target site resistance cases, and review crop selectivity mechanisms. Consistent and reproducible greenhouse screening and target-site mutation assays are necessary to effectively study and compare PPO-inhibitor resistance cases. To this end, we cover best practices in screening to accurately identify resistance ratios and properly interpret common screens for point mutations. The future of effective and sustainable PPO-inhibitor use relies on development of new chemistries that maintain activity on resistant biotypes and the promotion of responsible stewardship of PPO inhibitors both new and old. We present the biorational design of the new PPO inhibitor trifludimoxazin to highlight the future of PPO-inhibitor development and discuss the elements of sustainable weed control programs using PPO inhibitors, as well as how responsible stewardship can be incentivized. The sustained use of PPO inhibitors in future agriculture relies on the effective and timely communication from mode of action and resistance research to agronomists, Extension workers, and farmers.

This study evaluated the effects of dietary myo-inositol (MI) on growth performance, antioxidant status and lipid metabolism of juvenile Chinese mitten crab (Eriocheir sinensis) fed different percentage of lipid. Crabs (4·58 (sem 0·05) g) were fed four diets including a normal lipid diet (N, containing 7 % lipid and 0 mg/kg MI), N with MI supplementation (N + MI, containing 7 % lipid and 1600 mg/kg MI), a high lipid diet (H, containing 13 % lipid and 0 mg/kg MI) and H with MI supplementation (H + MI, containing 13 % lipid and 1600 mg/kg MI) for 8 weeks. The H + MI group showed higher weight gain and specific growth rate than those in the H group. The dietary MI could improve the lipid accumulations in the whole body, hepatopancreas and muscle as a result of feeding on the high dietary lipid (13 %) in crabs. Besides, the crabs fed the H + MI diets increased the activities of antioxidant enzymes but reduced the malondialdehyde content in hepatopancreas compared with those fed the H diets. Moreover, dietary MI enhanced the expression of genes involved in lipid oxidation and exportation, yet reduced lipid absorption and synthesis genes expression in the hepatopancreas of crabs fed the H diet, which might be related to the activation of inositol 1,4,5-trisphosphate receptor (IP3R)/calmodulin-dependent protein kinase kinase-β (CaMKKβ)/adenosine 5’-monophosphate-activated protein kinase (AMPK) signalling pathway. This study demonstrates that MI could increase lipid utilisation and reduce lipid deposition in the hepatopancreas of E. sinensis fed a high lipid diet through IP3R/CaMKKβ/AMPK activation. This work provides new insights into the function of MI in the diet of crustaceans.

This experiment was designed to investigate the effect of supplementing conjugated linoleic acid (CLA) in breeder hens diet on development and hepatic lipid metabolism of chick offspring. Hy-Line Brown breeder hens were allocated into two groups, supplemented with 0 (control (CT)) or 0·5 % CLA for 8 weeks. Offspring chicks were grouped according to the mother generation and fed for 7 d. CLA treatment had no significant influence on development, egg quality and fertility of breeder hens but darkened the egg yolks in shade and increased yolk sac mass compared with the CT group. Addition of CLA resulted in increased body mass and liver mass and decreased deposition of subcutaneous adipose tissue in chick offspring. The serum TAG and total cholesterol levels of chick offspring were decreased in CLA group. CLA treatment increased the incorporation of both CLA isomers (c9t11 and t10c12) in the liver of chick offspring, accompanied by the decreased hepatic TAG levels, related to the significant reduction of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) enzyme activities and the increased carnitine palmitoyltransferase-1 (CPT1) enzyme activity. Meanwhile, CLA treatment reduced the mRNA expression of genes related to fatty acid biosynthesis (FAS, ACC and sterol regulatory element-binding protein-1c) and induced the expression of genes related to β-oxidative (CPT1, AMP-activated protein kinase and PPARα) in chick offspring liver. In summary, the addition of CLA in breeder hens diet significantly increased the incorporation of CLA in the liver of chick offspring, which further regulate hepatic lipid metabolism.

In present study, we explored the effects and the underlying mechanisms of phospholipase C (PLC) mediating glucose-induced changes in intestinal glucose transport and lipid metabolism by using U-73122 (a PLC inhibitor). We found that glucose incubation activated the PLC signal and U-73122 pre-incubation alleviated the glucose-induced increase in plcb2, plce1 and plcg1 mRNA expression. Meanwhile, U-73122 pre-treatment blunted the glucose-induced increase in sodium/glucose co-transporters 1/2 mRNA and protein expressions. U-73122 pre-treatment alleviated the glucose-induced increase in TAG content, BODIPY 493/503 fluorescence intensity, lipogenic enzymes (glucose 6-phospate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), malic enzyme and fatty acid synthase (FAS)) activity and the mRNA expressions of lipogenic genes and related transcription factors (6pgd, g6pd, fas, acca, srebp1 and carbohydrate response element-binding protein (chrebp)) in intestinal epithelial cells of yellow catfish. Further research found that U-73122 pre-incubation mitigated the glucose-induced increase in the ChREBP protein expression and the acetylation level of ChREBP in HEK293T cells. Taken together, these data demonstrated that the PLC played a major role in the glucose-induced changes of glucose transport and lipid metabolism and provide a new perspective for revealing the molecular mechanism of glucose-induced changes of intestinal glucose absorption, lipid deposition and metabolism.

Dysregulation in hepatic lipid synthesis by excess dietary carbohydrate intake is often relevant with the occurrence of fatty liver; therefore, the thorough understanding of the regulation of lipid deposition and metabolism seems crucial to search for potential regulatory targets. In the present study, we examined TAG accumulation, lipid metabolism-related gene expression, the enzyme activities of lipogenesis-related enzymes, the protein levels of transcription factors or genes involving lipogenesis in the livers of yellow catfish fed five dietary carbohydrate sources, such as glucose, maize starch, sucrose, potato starch and dextrin, respectively. Generally speaking, compared with other carbohydrate sources, dietary glucose promoted TAG accumulation, up-regulated lipogenic enzyme activities and gene expressions, and down-regulated mRNA expression of genes involved in lipolysis and small ubiquitin-related modifier (SUMO) modification pathways. Further studies found that sterol regulatory element binding protein 1 (SREBP1), a key transcriptional factor relevant to lipogenic regulation, was modified by SUMO1. Mutational analyses found two important sites for SUMOylation modification (K254R and K264R) in SREBP1. Mutant SREBP lacking lysine 264 up-regulated the transactivation capacity on an SREBP-responsive promoter. Glucose reduced the SUMOylation level of SREBP1 and promoted the protein expression of SREBP1 and its target gene stearoyl-CoA desaturase 1 (SCD1), indicating that SUMOylation of SREBP1 mediated glucose-induced hepatic lipid metabolism. Our study elucidated the molecular mechanism of dietary glucose increasing hepatic lipid deposition and found that the SREBP-dependent transactivation was regulated by SUMO1 modification, which served as a new target for the transcriptional programmes governing lipid metabolism.

Maternal nutritional programming by a high-fat (HF) diet is related to hepatic lipid accumulation and steatosis in offspring. Conjugated linoleic acid (CLA) might ameliorate impaired hepatic lipid homoeostasis; therefore, the aim was to investigate the potential preventive effect of maternal CLA consumption on TAG metabolism alterations induced by HF diets in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed a control (C) diet, HF diet or HF diet supplemented with CLA (HF+CLA) for 4 weeks before mating and throughout pregnancy and lactation. After weaning, for 9 weeks, male offspring of C or HF rats continued with the same diets as their mothers (C/C or HF/HF groups, respectively) and male offspring of HF+CLA rats were fed HF or HF+CLA diets (HF+CLA/HF or HF+CLA/HF+CLA groups, respectively). Nutritional parameters, serum and liver TAG levels, the TAG secretion rate (TAG-SR) and the activities as well as gene expression of key hepatic enzymes involved in TAG regulation were assessed. The most interesting results were that maternal CLA decreased epididymal white adipose tissue weight and prevented serum and liver TAG accumulation induced by a HF diet in adult male offspring receiving or not receiving CLA. The prevention of liver steatosis in HF+CLA/HF+CLA and HF+CLA/HF offspring was associated with an increased hepatic TAG-SR. Overall, this study provides evidence that maternal CLA consumption programmes TAG regulation and in this way contributes to lowering lipid levels in tissues and preventing liver steatosis in particular.

The aim of the present study was to compare the effects of post-ruminally infused fat supplements, varying in fatty acid (FA) chain length, on animal performance, metabolism and milk FA. Eleven multiparous Holstein dairy cows were used in a replicated incomplete 3 × 3 Latin square design with 7-d periods, separated by 7-d washouts. Treatments were administered as abomasal infusions of enrichments providing 280 g/d of FA: (1) palmitic acid (98·4 % 16 : 0; PA), (2) caprylic and capric acids (56·2 % 8 : 0, 43·8 % 10 : 0; medium-chain TAG (MCT)) and (3) stearic acid (99·0 % 18 : 0; SA). Relative to PA, SA decreased the efficiency of fat-corrected milk production, which was associated with a tendency for higher DM intake and lower FA absorption with SA, whereas MCT was not different from PA for these variables. Milk fat concentration and yield were increased by PA relative to SA, but only fat yield tended to be greater relative to MCT. Relative to PA, MCT increased milk fat concentration of FA < 16 C, whereas SA increased FA > 16 C. Expression of mammary stearoyl-coA desaturase 1 was lower with SA than with PA. Relative to PA, liver expression of adenosine monophosphate-activated protein kinase-1 and pyruvate kinase was increased with MCT, whereas expression of these genes tended to be increased by SA. The mechanism of increased fat secretion with PA does not seem to be related to a modulation of the expression of lipogenesis-related genes, but rather to increased substrate availability as reflected by milk FA profile.

An oral starch administration trial was used to evaluate glucose homoeostasis in grass carp (Ctenopharyngodon idella) and Chinese longsnout catfish (Leiocassis longirostris Günther). Fish were administered with 3 g of a water and starch mixture (with 3:2 ratio) per 100 g body weight after fasting for 48 h. Fish were sampled at 0, 1, 3, 6, 12, 24 and 48 h after oral starch administration. In grass carp, plasma levels of glucose peaked at 3 h but returned to baseline at 6 h. However, in Chinese longsnout catfish, plasma glucose levels peaked at 6 h and returned to baseline at 48 h. The activity of intestinal amylase was increased in grass carp at 1 and 3 h, but no significant change in Chinese longsnout catfish was observed. The activity of hepatic glucose-6-phosphatase fell significantly in grass carp but change was not evident in Chinese longsnout catfish. The expression levels and enzymic activity of hepatic pyruvate kinase increased in grass carp, but no significant changes were observed in the Chinese longsnout catfish. Glycogen synthase (gys) and glycogen phosphorylase (gp) were induced in grass carp. However, there was no significant change in gys and a clear down-regulation of gp in Chinese longsnout catfish. In brief, compared with Chinese longsnout catfish, grass carp exhibited a rapid increase and faster clearance rate of plasma glucose. This effect was closely related to significantly enhanced levels of digestion, glycolysis, glycogen metabolism and glucose-induced lipogenesis in grass carp, as well as the inhibition of gluconeogenesis.

Bearded sprangletop [Diplachne fusca (L.) P. Beauv. ex Roem. & Schult. ssp. fascicularis (Lam.) P. M. Peterson & N. Snow] is a noxious annual grass weed of paddy fields, distributed in coastal regions of the Jiangsu and Hebei provinces in China. Cyhalofop-butyl has been widely used to control grass weeds since 2006 in China. Overreliance on cyhalofop-butyl has led to the evolution of resistant weeds. In this study, the resistance level and cyhalofop-butyl resistance mechanisms were investigated in the putative resistant (JSHH) population. The dose–response experiments showed that the JSHH D. fusca population had evolved 8.9-fold resistance to cyhalofop-butyl. Acetyl-CoA carboxylase (ACCase) sequencing revealed a point mutation (GGC to GCC) at amino acid position 2096, resulting in a Gly-2096-Ala substitution in the resistant population. To our knowledge, this is the first case of cyhalofop-butyl resistance in D. fusca and the first report of a target-site mutation conferring resistance to ACCase-inhibiting herbicides in D. fusca. In addition, the resistant D. fusca population (JSHH) with the Gly-2096-Ala mutation was cross-resistant to the aryloxyphenoxypropionate herbicide metamifop, the cyclohexanedione herbicide sethoxydim, and the phenylpyrazolin herbicide pinoxaden.

Conjugated linoleic acid (CLA) might regulate the lipid depots in liver and adipose tissue. As there is an association between maternal nutrition, fat depots and risk of offspring chronic disease, the aim was to investigate the effect of maternal CLA consumption on TAG regulation and some inflammatory parameters in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed control (C) or CLA-supplemented (1 %, w/w) diets during 4 weeks before and throughout pregnancy and lactation. After weaning, male offspring of CLA rats were fed C or CLA diets (CLA/C and CLA/CLA groups, respectively), whereas C male rat offspring were fed a C diet (C/C group) for 9 weeks. Serum TAG levels were increased in the CLA/CLA and CLA/C groups, associated with a reduction of lipoprotein lipase activity and weights of adipose tissue. The liver TAG levels were decreased in the CLA/CLA group, related to a significant reduction of fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) and glucose-6-phosphate dehydrogenase enzyme activities, as well as to the mRNA levels of FAS, ACC, stearoyl-CoA desaturase-1 and sterol regulatory element-binding protein-1c. Even though normal TAG levels were found in the liver of CLA/C rats, a reduction of lipogenesis was also observed. Thus, these results demonstrated a programming effect of CLA on the lipid metabolic pathways leading to a preventive effect on the TAG accretion in adipose tissue and the liver of male rat offspring. This knowledge could be important to develop some dietary strategies leading to a reduced incidence of obesity and fatty acid liver disease in humans.

Perinatal maternal high-fat (HF) diet programmes offspring obesity. Obesity is associated with overactivation of the endocannabinoid system (ECS) in adult subjects, but the role of the ECS in the developmental origins of obesity is mostly unknown. The ECS consists of endocannabinoids, cannabinoid receptors (cannabinoid type-1 receptor (CB1) and cannabinoid type-2 receptor (CB2)) and metabolising enzymes. We hypothesised that perinatal maternal HF diet would alter the ECS in a sex-dependent manner in white and brown adipose tissue of rat offspring at weaning in parallel to obesity development. Female rats received standard diet (9 % energy content from fat) or HF diet (29 % energy content from fat) before mating, during pregnancy and lactation. At weaning, male and female offspring were killed for tissue harvest. Maternal HF diet induced early obesity, white adipocyte hypertrophy and increased lipid accumulation in brown adipose tissue associated with sex-specific changes of the ECS’s components in weanling rats. In male pups, maternal HF diet decreased CB1 and CB2 protein in subcutaneous adipose tissue. In female pups, maternal HF diet increased visceral and decreased subcutaneous CB1. In brown adipose tissue, maternal HF diet increased CB1 regardless of pup sex. In addition, maternal HF diet differentially changed oestrogen receptor across the adipose depots in male and female pups. The ECS and oestrogen signalling play an important role in lipogenesis, adipogenesis and thermogenesis, and we observed early changes in their targets in adipose depots of the offspring. The present findings provide insights into the involvement of the ECS in the developmental origins of metabolic disease induced by inadequate maternal nutrition in early life.

A maternal high-fat, high-sucrose (HFS) diet alters offspring glucose and lipid homoeostasis through unknown mechanisms and may be modulated by folic acid. We investigated the effect of a maternal HFS diet on glucose homoeostasis, expression of genes and proteins associated with insulin signalling and lipid metabolism and the effect of prenatal folic acid supplementation (HFS/F) in male rat offspring. Pregnant Sprague–Dawley rats were randomly fed control (CON), HFS or HFS/F diets. Offspring were weaned on CON; at postnatal day 70, fasting plasma insulin and glucose and liver and skeletal muscle gene and protein expression were measured. Treatment effects were assessed by one-way ANOVA. Maternal HFS diet induced higher fasting glucose in offspring v. HFS/F (P=0·027) and down-regulation (P<0·05) of genes coding for v-Akt murine thymoma viral oncogene homolog 2, resistin and v-Raf-1 murine leukaemia viral oncogene homolog 1 (Raf1) in offspring skeletal muscle and acetyl-CoA carboxylase (Acaca), fatty acid synthase and phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit β in offspring liver. Skeletal muscle neuropeptide Y and hepatic Kruppel-like factor 10 were up-regulated in HFS v. CON offspring (P<0·05). Compared with CON, Acaca and Raf1 protein expression levels were significantly lower in HFS offspring. Maternal HFS induced higher homoeostasis model of assessment index of insulin resistance v. CON (P=0·030) and HFS/F was associated with higher insulin (P=0·016) and lower glucose (P=0·025). Maternal HFS diet alters offspring insulin sensitivity and de novo hepatic lipogenesis via altered gene and protein expression, which appears to be potentiated by folate supplementation.

The present study explored the mechanisms of dietary Zn influencing Zn and lipid deposition in the fore- and mid- intestine in yellow catfish Pelteobagrus fulvidraco, and investigated whether the mechanism was intestinal-region dependent. For this purpose, yellow catfish were fed three diets containing Zn levels of 8·83, 19·20 and 146·65 mg Zn/kg, respectively. Growth performance, intestinal TAG and Zn contents as well as activities and mRNA expression of enzymes and genes involved in Zn transport and lipid metabolism in the fore- and mid-intestine were analysed. Dietary Zn increased Zn accumulation as well as activities of Cu-, Zn-superoxide dismutase and ATPase in the fore- and mid-intestine. In the fore-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, metallothionein (MT) and metal response element-binding transcription factor-1 (MTF-1), but down-regulated mRNA levels of ZIP4 and ZIP5. In the mid-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, MT and MTF-1, but down-regulated mRNA levels of ZIP4 and ZIP5. Dietary Zn reduced TAG content, down-regulated activities of 6-phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME) and fatty acid synthase (FAS) activities, and reduced mRNA levels of 6PGD, G6PD, FAS, PPARγ and sterol-regulator element-binding protein (SREBP-1), but up-regulated mRNA levels of carnitine palmitoyltransferase IA, hormone-sensitive lipase (HSLa), adipose TAG lipase (ATGL) and PPARα in the fore-intestine. In the mid-intestine, dietary Zn reduced TAG content, activities of G6PD, ME, isocitrate dehydrogenase and FAS, down-regulated mRNA levels of 6PGD, G6PD, FAS, acetyl-CoA carboxylase a, PPARγ and SREBP-1, but up-regulated mRNA expression of HSLa, ATGL and PPARγ. The reduction in TAG content following Zn addition was attributable to reduced lipogenesis and increased lipolysis, and similar regulatory mechanisms were observed between the fore- and mid-intestine.

Greenhouse and laboratory experiments were conducted to determine the effect of DPX-PE350 on the herbicidal activity of fluazifop-P on large crabgrass. Greenhouse experiments indicated that fluazifop-P activity was antagonized by DPX-PE350. This antagonism was reduced by increasing fluazifop-P rates or by applying DPX-PE350 after fluazifop-P. Applying DPX-PE350 24 h prior to fluazifop-P reduced fluazifop-P activity more than applying it 10 min prior. The effect of DPX-PE350 application to large crabgrass on extractable acetyl-CoA carboxylase activity, and the effect of DPX-PE350 on acetyl-CoA carboxylase activity in vitro also was studied. Applying DPX-PE350 to large crabgrass prior to protein extraction did not reduce fluazifop-P inhibition of acetyl CoA carboxylase activity in vitro. The presence of DPX-PE350 in the enzyme assay mix did not affect fluazifop-P inhibition of acetyl-CoA carboxylase activity. The effect of DPX-PE350 on uptake, translocation, and metabolism of fluazifop-P was considered. DPX-PE350 did not affect uptake of fluazifop-P by large crabgrass. Applying DPX-PE350 24 h prior to fluazifop-P decreased translocation of fluazifop-P out of the treated leaf 44 to 53% whereas mixing DPX-PE350 with fluazifop-P decreased fluazifop-P translocation only 15 to 17%. Metabolism of fluazifop-P was not affected by applications of DPX-PE350. These studies suggest that the antagonism of fluazifop-P activity by DPX-PE350 is due to decreased translocation of fluazifop-P out of the treated leaf.

Inheritance of resistance to diclofop was studied in three wild oat biotypes (designated B, C., and H) from the Willamette Valley of Oregon. Cultivated oat (cultivar ‘Monida’) was crossed, including reciprocals, to three wild oat biotypes. Leaves of each F1 plant were spotted with diclofop as a nondestructive test for resistance or susceptibility. All F1 hybrids were resistant, indicating that resistance is dominant and is under nuclear control. The F2 plants where Monida was the maternal parent were screened with diclofop, and F2 plants of the Monida/C cross were screened with fenoxaprop because the parent C biotype was resistant to fenoxaprop. At lower doses, a 3:1 (R:S) segregation ratio in F2 was observed and at higher doses a 1:3 (R:S) segregation ratio was often observed. The F2:3 families segregated in a 1:2:1 (all resistant : segregating resistant and susceptible all susceptible) ratio when treated with a 1.1-kg ae ha−1 dose of diclofop. This confirms that resistance to diclofop in the B, C, and H biotypes is primarily under monogenic control, with resistance being dominant to susceptibility at lower herbicide doses. At increased doses, susceptibility becomes dominant. Knowledge of the inheritance of resistance may help in the development of containment measures to prevent the spread of herbicide-resistance genes.

A diclofop-methyl-resistant biotype of Italian ryegrass was characterized to determine the expression and inheritance of herbicide resistance and whether this trait was due to the presence of a diclofop-insensitive form of acetyl-coenzyme A carboxylase (ACCase). At the whole plant level, the resistant biotype was > 93-fold more resistant to diclofop-methyl than the susceptible biotype. Crosses of diclofop-resistant and –susceptible plants were performed to produce F1 plants. No maternal effects were evident in responses of reciprocal F1 plants to diclofop. GR50 diclofop rates determined for resistant, F1, and susceptible plants were 15, 6.3, and 0.16 kg ha−1, respectively. F2 populations treated with a 7.5 kg ha−1 rate of diclofop exhibited three injury response phenotypes 3 wk after treatment: a susceptible (S) phenotype which was killed, an intermediate resistance (I) phenotype with severe injury, and a resistant (R) phenotype with little or no injury. Testcross progeny exhibited only I and S phenotypes. Observed segregation of phenotypes in F2 and testcross populations conformed to segregation ratios predicted for a trait with inheritance controlled by a single partially dominant nuclear gene. ACCase activity determined in crude cell-free extracts of resistant, F1, and susceptible biotypes exhibited I50 values of 50, 20, and 0.7 μM diclofop, respectively. A positive relationship between the injury response phenotype and site of action (ACCase) response to diclofop was evident in both F1 and F2 populations. In extracts from R, I, and S phenotype F2 plants, 20 μM diclofop acid inhibited ACCase-mediated incorporation of 14C by 27.1, 45.1, and 78.9%, respectively. The ACCase data are consistent with the hypothesis that diclofop resistance in Italian ryegrass is conferred by a diclofop-insensitive form of ACCase.

The aryloxyphenoxypropionate and cyclohexanedione herbicides, which inhibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypothesized to act at specific sites on the plasmalemma. An impermeant sulfhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (Em) in rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the Em response, and the repolarization of Em in herbicide-resistant rigid ryegrass following removal of diclofop acid also provide support for this hypothesis. However, similar membrane responses in resistant grasses and broadleaf species suggest that the membrane response may not be important in the phytotoxic activity of the postemergence graminicides under field conditions. In addition, an antagonistic interaction was not observed in roots of susceptible grasses exposed to combinations of diclofop-methyl and 2,4-D. Furthermore, the repolarization of the Em in diclofop-resistant rigid ryegrass was correlated to differential acidification of the external solution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the membrane response is probably not involved in herbicide phytotoxicity in agricultural systems, a higher extracellular pH in the resistant biotypes of rigid ryegrass may inhibit the movement of these weak-acid herbicides across the plasmalemma, and possibly contribute to increased herbicide tolerance.

Five classes of herbicides (carbamothioates, chloroacetamides, substituted pyridazinones, cyclohexanediones, and aryloxyphenoxypropionic acids) have been reported to inhibit lipid biosynthesis in higher plants. Carbamothioates impair the synthesis of surface lipids (waxes, cutin, suberin). These effects have been attributed to the ability of this herbicide class to inhibit one or more acyl-CoA elongases. Though as yet poorly characterized, these enzymes are associated with the endoplasmic reticulum and catalyze the condensation of malonyl-CoA with fatty acid acyl-CoA substrates to form very long-chain fatty acids used in the synthesis of surface lipids. There is contradictory evidence regarding the effects of chloroacetamide herbicides on de novo fatty acid biosynthesis. Selected substituted pyridazinones decrease the degree of unsaturation of plastidic galactolipids. This effect is attributed to the ability of selected members of this herbicide class to inhibit fatty acid desaturases which are thought to be located in the chloroplast envelope. Aryloxyphenoxypropionic acid and cyclohexanedione herbicides inhibit de novo fatty acid biosynthesis in grasses. The target site for these herbicide classes is the enzyme acetyl-CoA carboxylase which is found in the stroma of plastids. In most cases, selectivity between grasses and dicots is expressed at this site. Aryloxyphenoxypropionic acids and cyclohexanediones are reversible, linear, noncompetitive inhibitors of acetyl-CoA carboxylase from grasses. Both classes are also mutually exclusive inhibitors of grass acetyl-CoA carboxylase which suggests that they bind at a common domain on the enzyme.

Keng stiffgrass is a serious farmland grass weed distributed globally in winter wheat fields and rice–wheat double-cropping areas. The intensive use of acetyl-CoA carboxylase (ACCase)-inhibiting herbicides has led to the evolution of resistance in a growing number of grass weeds. In this study, whole-plant pot bioassay experiments were conducted to establish that a Keng stiffgrass population from eastern China, JYJD-2, has evolved high-level resistance to fenoxaprop-P-ethyl and moderate resistance to quizalofop-P-ethyl and pinoxaden. Using the derived cleaved amplified polymorphic sequence method, a tryptophan-to-cysteine mutation at codon position 1999 (W1999C) was detected in the ACCase gene of the resistant population JYJD-2. Of the 100 JYJD-2 plants tested, we found 47 heterozygous resistant and 53 homozygous sensitive individuals. In vitro ACCase assays revealed that the IC50 value of the ACCase activity of the resistant population JYJD-2 was 6.48-fold higher than that of the susceptible population JYJD-1. To the best of our knowledge, this is the first report of the occurrence of W1999C mutation in the ACCase gene of fenoxaprop-P-ethyl–resistant Keng stiffgrass. This study confirmed the resistance of Keng stiffgrass to the ACCase inhibitor fenoxaprop-P-ethyl, cross-resistance to other ACCase inhibitors, and the resistance being conferred by specific ACCase point mutations at amino acid position 1999.