Nontarget-site resistance due to rapid physiological response in 2,4-D resistant Conyza sumatrensis: Reduced 2,4-D translocation and auxin-induced gene expression
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ABSTRACT:
ORGANISM(S): Conyza sumatrensis
PROVIDER: GSE226337 | GEO | 2023/06/30
REPOSITORIES: GEO
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Project description:The synthetic auxin 2,4-dichlorophenoxyacetic acid (2,4-D) functions as an agronomic weed control herbicide. High concentrations of 2,4-D induce plant growth defects, particularly leaf epinasty and stem curvature. Although the 2,4-D phenotype is associated with ROS production, little is known about ROS-dependent signalling. In this study, by using T-DNA Arabidopsis mutants to silence peroxisomal acyl CoA oxidase 1 (acx1-2), we identified ACX1 as one of the main sources of ROS production and as partly the cause of the epinasty phenotype following the application of 2,4-D. Transcriptomic analyses of WT plants after treatment with 2,4-D revealed a ROS-related peroxisomal footprint in early plant responses, while other organelles, such as mitochondria and chloroplasts, are involved in later responses. Interestingly, a group of ACX1-dependent transcripts in plant responses to 2,4-D, previously associated with epinasty, is related to auxin biosynthesis, metabolism and signalling. We found that protein AUXIN SIGNALING F-BOX 3 (AFB3), a component of SCF (ASK-cullin-F-box) E3 ubiquitin ligase complexes, which functions as an auxin receptor and mediates Aux/IAA proteasomal degradation, acts downstream of ACX1 and is involved in the epinasty phenotype induced by 2,4-D. We also found that protein degradation associated with ubiquitin E3-RING and E3-SCF-FBOX in ACX1-dependent signalling in plant responses to 2,4-D is significantly regulated over longer treatment periods.
2021-12-01 | GSE179303 | GEO
Project description:This experiment was annotated by TAIR (http://www.arabidopsis.org). In this experiment we examined whole genome response to herbicidal levels of 2,4-D application. Arabidopsis plants (14 days) grown in vitro on MS medium in petri dishes were flooded with 1 mL stock of 2,4-D to enable root uptake. Plants were treated with 1.0 mM 2,4-D for a period of 1 hour immediately after which RNA was extracted and used for the microarray based experiments. the goal of this study was to explore the herbicidal mode of action of auxinic herbicide 2,4-D. Experimenter name = Chitra Raghavan Experimenter department = Trevor Stevenson Laboratory Experimenter institute = IRRI Experimenter address = Entomology and Plant Pathology Division IRRI Experimenter zip/postal_code = Manila 4031 Experimenter country = Philippines Keywords: compound_treatment_design
2007-01-08 | GSE5743 | GEO
Project description:This experiment was annotated by TAIR (http://www.arabidopsis.org). In this experiment we examined whole genome response to herbicidal levels of 2,4-D application. Arabidopsis plants (14 days) grown in vitro on MS medium in petri dishes were flooded with 1 mL stock of 2,4-D to enable root uptake. Plants were treated with 1.0 mM 2,4-D for a period of 1 hour immediately after which RNA was extracted and used for the microarray based experiments. the goal of this study was to explore the herbicidal mode of action of auxinic herbicide 2,4-D. Experimenter name = Chitra Raghavan; Experimenter department = Trevor Stevenson Laboratory; Experimenter institute = IRRI; Experimenter address = Entomology and Plant Pathology Division IRRI; Experimenter zip/postal_code = Manila 4031; Experimenter country = Philippines Experiment Overall Design: 3 samples were used in this experiment
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Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.
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Project description:The use of a systems biology approach to analyze common and specific mechanisms of liver toxicity induced by munitions compounds TNT, 2,6-DNT, 2,4-DNT, 4A-DNT, and 2A-DNT The munitions compound 2,4,6-trinitrotoluene (TNT), its environmental degradation products 2-amino-4,6-dinitrotoluene (2A-DNT) and 4-amino-2,6-dinitrotoulene (4A-DNT), and two other munitions, 2,4-dinitrotoluene (2,4-DNT) and 2,4-dinitrotoluene (2,6-DNT) contaminate contaminate land, water and retired ammunitions plants. The release of these compounds to the environment is due to military activities and a series of manufacturing processes. Although toxicity has been characterized for these compounds, little is known of their mechanism of action. Here we describe to use an integrative systems biology approach including toxicology, pathology, transcriptomics, metabolomics, gene function classification, pathway analysis and gene network modeling to try to understand the mechanisms of toxicity of these compounds.
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Project description:In this study we treated Brachypodium distachyon roots with synthetic auxin, 2,4-D, to induce nodule-like structures (NLS) and performed RNA-seq to assess transcriptome changes during NLS formation.
2018-04-22 | GSE97940 | GEO
Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.
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2014-06-30 | E-GEOD-50167 | biostudies-arrayexpress