Flufenacet activity is affected by GST inhibitors in blackgrass (Alopecurus myosuroides) populations with reduced flufenacet sensitivity and higher expression levels of GSTs

AbstractThe WSSA Group 15 (HRAC Group K3) herbicide flufenacet is a key compound in weed resistance management, primarily used for PRE control of grass weeds in winter cereal–based crop rotations in Europe. Although resistance to compounds of its mechanism of action (inhibition of the synthesis of very-long-chain fatty acids) generally evolves slowly, reduced flufenacet efficacy due to enhanced glutathione transferase (GST) activity has been described in several blackgrass (Alopecurus myosuroides Huds.) populations. The present study aimed to better understand of the mechanism of flufenacet detoxification in A. myosuroides. Therefore, we characterized four A. myosuroides populations with different levels of flufenacet sensitivity. Flufenacet degradation was significantly slowed down in a sensitive population and a population with reduced flufenacet sensitivity by the use of the GST inhibitors tridiphane and ethacrynic acid at sublethal rates. Finally, an RNA sequencing (RNA-seq) study with the four A. myosuroides populations was conducted. In total, six differentially expressed GSTs and nine transcription factors as well as a keto-acyl-CoA reductase involved in the biosynthesis of very-long-chain fatty acids were identified as candidate genes among a set of 319 significantly more highly expressed gene-associated contigs. Among a set of 218 contigs with significantly lower expression levels, receptor kinase activity was the most frequent annotation. In summary, the likely GST-mediated reduction in sensitivity evolves in A. myosuroides at a slow rate and can partially be reversed by an interaction between flufenacet and the GST inhibitors tridiphane and ethacrynic acid. This provides further evidence for enhanced GST activity as a key mechanism in flufenacet resistance in A. myosuroides and supports the hypothesis that the six differentially expressed GSTs detected in the present RNA-seq study are potentially involved in flufenacet resistance.

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Epigenomics and Lipidomics Integration in Alzheimer Disease: Pathways Involved in Early Stages

Biomedicines ◽

10.3390/biomedicines9121812 ◽

2021 ◽

Vol 9 (12) ◽

pp. 1812

Author(s):

Carmen Peña-Bautista ◽

Lourdes Álvarez-Sánchez ◽

Antonio José Cañada-Martínez ◽

Miguel Baquero ◽

Consuelo Cháfer-Pericás

Keyword(s):

Fatty Acids ◽

Alzheimer Disease ◽

Target Genes ◽

Differentially Expressed ◽

Long Chain Fatty Acids ◽

Targeted Analysis ◽

Fatty Acids Metabolism ◽

Positive Correlations ◽

Long Chain ◽

Chain Fatty Acids

Background: Alzheimer Disease (AD) is the most prevalent dementia. However, the physiopathological mechanisms involved in its development are unclear. In this sense, a multi-omics approach could provide some progress. Methods: Epigenomic and lipidomic analysis were carried out in plasma samples from patients with mild cognitive impairment (MCI) due to AD (n = 22), and healthy controls (n = 5). Then, omics integration between microRNAs (miRNAs) and lipids was performed by Sparse Partial Least Squares (s-PLS) regression and target genes for the selected miRNAs were identified. Results: 25 miRNAs and 25 lipids with higher loadings in the sPLS regression were selected. Lipids from phosphatidylethanolamines (PE), lysophosphatidylcholines (LPC), ceramides, phosphatidylcholines (PC), triglycerides (TG) and several long chain fatty acids families were identified as differentially expressed in AD. Among them, several fatty acids showed strong positive correlations with miRNAs studied. In fact, these miRNAs regulated genes implied in fatty acids metabolism, as elongation of very long-chain fatty acids (ELOVL), and fatty acid desaturases (FADs). Conclusions: The lipidomic–epigenomic integration showed that several lipids and miRNAs were differentially expressed in AD, being the fatty acids mechanisms potentially involved in the disease development. However, further work about targeted analysis should be carried out in a larger cohort, in order to validate these preliminary results and study the proposed pathways in detail.

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Diet supplemented with medium- and long-chain fatty acids does not affect lower GI motility and visceral pain in rats

10.26226/morressier.59a6b345d462b80290b5487f ◽

2017 ◽

Author(s):

Paula Mosinska

Keyword(s):

Fatty Acids ◽

Visceral Pain ◽

Long Chain Fatty Acids ◽

Long Chain ◽

Chain Fatty Acids ◽

Gi Motility

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Binding of bilirubin and long-chain fatty acids to human serum albumin with general remarks on displacement of firmly bound ligands

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.3109/00365517709091491 ◽

1977 ◽

Vol 37 (3) ◽

pp. 257-266 ◽

Cited By ~ 8

Author(s):

R. Brodersen ◽

L. Funding

Keyword(s):

Fatty Acids ◽

Human Serum Albumin ◽

Serum Albumin ◽

Human Serum ◽

Long Chain Fatty Acids ◽

Long Chain ◽

Chain Fatty Acids

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Differential Effects of Fatty Acid Saturation and Chain Length on NASH in Juvenile Iberian Pigs

Current Developments in Nutrition ◽

10.1093/cdn/nzaa050_005 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 682-682 ◽

Cited By ~ 1

Author(s):

Kayla Dillard ◽

Morgan Coffin ◽

Gabriella Hernandez ◽

Victoria Smith ◽

Catherine Johnson ◽

...

Keyword(s):

Fatty Acids ◽

Body Weight ◽

Fatty Acid ◽

Liver Injury ◽

Olive Oil ◽

Coconut Oil ◽

Long Chain Fatty Acids ◽

Medium Chain ◽

Long Chain ◽

Chain Fatty Acids

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons < 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.

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