Influence of water temperature on the efficacy of diquat and endothall versus curlyleaf pondweed

determine the impact of water temperature on the efficacy of the contact herbicides diquat (6,7-dihydrodipyrido [1,2- α:2’,1’-c] pyrazinediium ion) and endothall (7-oxabicyclo [2.2.1] heptane-2,3-dicarboxylic acid) for control of the exotic nuisance species curlyleaf pondweed (Potamogeton crispus L.) across a range of water temperatures

\u3ci\u3eIn silico\u3c/i\u3e identification of genetic mutations conferring resistance to acetohydroxyacid synthase inhibitors: A case study of \u3ci\u3eKochia scoparia\u3c/i\u3e

Mutations that confer herbicide resistance are a primary concern for herbicide-based chemical control of invasive plants and are often under-characterized structurally and functionally. As the outcome of selection pressure, resistance mutations usually result from repeated long-term applications of herbicides with the same mode of action and are discovered through extensive field trials. Here we used acetohydroxyacid synthase (AHAS) of Kochia scoparia (KsAHAS) as an example to demonstrate that, given the sequence of a target protein, the impact of genetic mutations on ligand binding could be evaluated and resistance mutations could be identified using a biophysics-based computational approach. Briefly, the 3D structures of wild-type (WT) and mutated KsAHAS-herbicide complexes were constructed by homology modeling, docking and molecular dynamics simulation. The resistance profile of two AHAS-inhibiting herbicides, tribenuron methyl and thifensulfuron methyl, was obtained by estimating their binding affinity with 29 KsAHAS (1 WT and 28 mutated) using 6 molecular mechanical (MM) and 18 hybrid quantum mechanical/molecular mechanical (QM/MM) methods in combination with three structure sampling strategies. By comparing predicted resistance with experimentally determined resistance in the 29 biotypes of K. scoparia field populations, we identified the best method (i.e., MM-PBSA with single structure) out of all tested methods for the herbicide-KsAHAS system, which exhibited the highest accuracy (up to 100%) in discerning mutations conferring resistance or susceptibility to the two AHAS inhibitors. Our results suggest that the in silico approach has the potential to be widely adopted for assessing mutation-endowed herbicide resistance on a case-by-case basis

Molecular evolution of herbicide resistance to phytoene desaturase inhibitors in \u3ci\u3eHydrilla verticillata\u3c/i\u3e and its potential use to generate herbicide-resistant crops

Hydrilla [Hydrilla verticillata (Lf) Royle] is one of the most serious invasive aquatic weed problems in the USA. This plant possesses numerous mechanisms of vegetative reproduction that enable it to spread very rapidly. Management of this weed has been achieved by the systemic treatment of water bodies with the herbicide fluridone. At least three dioecious fluridone-resistant biotypes of hydrilla with two- to fivefold higher resistance to the herbicide than the wild-type have been identified. Resistance is the result of one of three independent somatic mutations at the arginine 304 codon of the gene encoding phytoene desaturase, the molecular target site of fluridone. The specific activities of the three purified phytoene desaturase variants are similar to the wild-type enzyme. The appearance of these herbicideresistant biotypes may jeopardize the ability to control the spread of this non-indigenous species to other water bodies in the southern USA. The objective of this paper is to provide general information about the biology and physiology of this aquatic weed in relation to its recent development of resistance to the herbicide fluridone, and to discuss how this discovery might lead to a new generation of herbicide-resistant crops

Molecular evolution of herbicide resistance to phytoene desaturase inhibitors in \u3ci\u3eHydrilla verticillata\u3c/i\u3e and its potential use to generate herbicide-resistant crops

Hydrilla [Hydrilla verticillata (Lf) Royle] is one of the most serious invasive aquatic weed problems in the USA. This plant possesses numerous mechanisms of vegetative reproduction that enable it to spread very rapidly. Management of this weed has been achieved by the systemic treatment of water bodies with the herbicide fluridone. At least three dioecious fluridone-resistant biotypes of hydrilla with two- to fivefold higher resistance to the herbicide than the wild-type have been identified. Resistance is the result of one of three independent somatic mutations at the arginine 304 codon of the gene encoding phytoene desaturase, the molecular target site of fluridone. The specific activities of the three purified phytoene desaturase variants are similar to the wild-type enzyme. The appearance of these herbicideresistant biotypes may jeopardize the ability to control the spread of this non-indigenous species to other water bodies in the southern USA. The objective of this paper is to provide general information about the biology and physiology of this aquatic weed in relation to its recent development of resistance to the herbicide fluridone, and to discuss how this discovery might lead to a new generation of herbicide-resistant crops

Cannabinoid (CB2) Receptor Deficiency Reduces the Susceptibility of Macrophages to Oxidized LDL/Oxysterol-Induced Apoptosis

Macrophage apoptosis is an important process in the pathophysiology of atherosclerosis. Oxidized low-density lipoproteins (OxLDL) are a major component of lesions and potently induce macrophage apoptosis. Cannabinoid receptor 2 (CB2), the predominant macrophage cannabinoid receptor, modulates several macrophage processes associated with ongoing atherosclerosis; however, the role of CB2 in macrophage apoptosis is unknown. To determine if CB2 influences a macrophage apoptotic pathway relevant to atherosclerosis, we examined the effect of CB2 deficiency on OxLDL-induced macrophage apoptosis. In situ terminal transferase-mediated dUTP nick end labeling (TUNEL) analysis of resident peritoneal macrophages detected significantly fewer apoptotic CB2-/- macrophages than CB2+/+ macrophages after incubation with OxLDL (27.9 ± 4.7% vs. 61.9 ± 8.5%, P \u3c 0.001) or 7-ketocholesterol (7KC) (18.9 ± 10.5% vs. 54.1 ± 6.9%, P \u3c 0.001), an oxysterol component of OxLDL. Caspase-3 activity; proteolytic conversion of procaspase-3; and cleavage of a caspase-3 substrate, PARP, were also diminished in 7KC-treated CB2-/-macrophages. Furthermore, the deactivation of the prosurvival kinase, Akt, in response to 7KC was impaired in CB2-/-macrophages. These results suggest that CB2 expression increases the susceptibility of macrophages to OxLDL-induced apoptosis, in part, by modulating the effect of oxysterols on the Akt survival pathway and that CB2 may influence atherosclerosis by modulating lesional macrophage apoptosis

Temperature-dependent development, cold tolerance, and potential distribution of cricotopus lebetis (Diptera: Chironomidae), a tip miner of hydrilla verticillata (Hydrocharitaceae)

© The Author 2014. Published by Oxford University Press on behalf of the Entomological Society of America. A chironomid midge, Cricotopus lebetis (Sublette) (Diptera: Chironomidae), was discovered attacking the apical meristems of Hydrilla verticillata (L.f. Royle) in Crystal River, Citrus Co., Florida in 1992. The larvae mine the stems of H. verticillata and cause basal branching and stunting of the plant. Temperature-dependent development, cold tolerance, and the potential distribution of the midge were investigated. The results of the temperature-dependent development study showed that optimal temperatures for larval development were between 20 and 30°C, and these data were used to construct a map of the potential number of generations per year of C. lebetis in Florida. Data from the cold tolerance study, in conjunction with historical weather data, were used to generate a predicted distribution of C. lebetis in the United States. A distribution was also predicted using an ecological niche modeling approach by characterizing the climate at locations where C. lebetis is known to occur and then finding other locations with similar climate. The distributions predicted using the two modeling approaches were not significantly different and suggested that much of the southeastern United States was climatically suitable for C. lebetis

A Thousand Contradictory Ways: Addiction, Neuroscience, and Expert Autobiography

Neuroscientific accounts of addiction are increasingly influential in health and medical circles. At the same time a diverse, if equally scientifically focused, opposition to addiction neuroscience is emerging. In this struggle over the merits of addiction neuroscience are elements of a uniquely 21st-century public engagement with science. No longer trusted by the public as the unerring source of objective knowledge about the world, science is, at least in some contexts, increasingly treated as just one voice among many. Observing the difficulties this loss of faith in science poses for effective action on pressing issues such as climate change, philosopher Bruno Latour develops a different (ecological) approach to scientific knowledge, one that for the first time allows scientists (and other “moderns”) to understand it for what it really is and locate it “diplomatically” alongside other modes of knowing. In this article, I ask whether a similar innovation is needed to allow more effective understanding of addiction. I explore this question by analyzing two recent, widely discussed, popular books (Marc Lewis’s Memoirs of an Addicted Brain: A Neuroscientist Examines His Former Life on Drugs, 2011 and Carl Hart’s High Price: A Neuroscientist’s Journey of Self-discovery that Challenges Everything You Think You Know About Drugs and Society, 2013) as well as reviews of these books. Written by neuroscientists, and drawing heavily on personal memoir to illustrate and ratify their competing views on drugs and addiction, both books crystallize contemporary dilemmas about science, empiricism, and the nature of evidence and truth. How are we to understand their mix of “scientific fact” and individual self-observation, what does this mix suggest about scientific knowledge, and what are its implications for dominant notions of “evidence-based” drug policy and treatment? I argue that these books both trouble and reinforce our taken-for-granted distinctions between science and personal stories, between objectivity and subjectivity, and note the lost opportunities the books represent for a more searching and productive (Latour might say “ecological”) engagement with science