Paraquat Resistance of Weeds - the Case of Conyza canadensis (L.) Cronq

The paper gives an overview of literature on paraquat resistance of weeds and the proposed mechanism of resistance. New results we achieved on horseweed ( Conyza canadensis /L./, Cronq.) are discussed in detail. It was demonstrated that there is no significant constitutive difference related to the paraquat resistance between untreated susceptible and paraquat-resistant horseweed plants. The lower sensitivity of flowering resistant plants may be due to the fact that paraquat content in treated leaves of flowering resistant plants was only 25% as compared to those measured at rosette stage. Our results confirm that paraquat resistance is not based on elevated level and activity of antioxidant enzyme system. The hypothesized role of polyamines in the resistance mechanisms can be excluded. The higher putrescine and total polyamine content of paraquat treated resistant leaves can rather be regarded as a general stress response, than as a symptom of paraquat resistance. A paraquat-inducible protein is supposed to play a role in the resistance, which presumably functions by binding paraquat to an inactivating site and/ or by carrying paraquat to metabolically inactive cell compartment (vacuole, cell wall). From model experiments it is concluded that paraquat and diquat preferentially form hydrophylic interactions with proteins containing a higher amount of lysine and glutamic acid. Consequently, the reason for paraquat resistance in horseweed is probably a hydrophylic interaction of paraquat with a protein, leading to inactivation of paraquat through forming a conjugate and/or sequestration into the vacuole or the cell wall.

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Sorting out the Superbugs: Potential of Sortase A Inhibitors among Other Antimicrobial Strategies to Tackle the Problem of Antibiotic Resistance

Antibiotics ◽

10.3390/antibiotics10020164 ◽

2021 ◽

Vol 10 (2) ◽

pp. 164 ◽

Cited By ~ 1

Author(s):

Nikita Zrelovs ◽

Viktorija Kurbatska ◽

Zhanna Rudevica ◽

Ainars Leonchiks ◽

Davids Fridmanis

Keyword(s):

Cell Wall ◽

Antibiotic Resistance ◽

Pathogenic Bacteria ◽

Resistance Mechanisms ◽

Surface Proteins ◽

Sortase A ◽

Inhibitory Compounds ◽

Alternative Means ◽

Alternative Approaches ◽

Conventional Antibiotics

Rapid spread of antibiotic resistance throughout the kingdom bacteria is inevitably bringing humanity towards the “post-antibiotic” era. The emergence of so-called “superbugs”—pathogen strains that develop resistance to multiple conventional antibiotics—is urging researchers around the globe to work on the development or perfecting of alternative means of tackling the pathogenic bacteria infections. Although various conceptually different approaches are being considered, each comes with its advantages and drawbacks. While drug-resistant pathogens are undoubtedly represented by both Gram(+) and Gram(−) bacteria, possible target spectrum across the proposed alternative approaches of tackling them is variable. Numerous anti-virulence strategies aimed at reducing the pathogenicity of target bacteria rather than eliminating them are being considered among such alternative approaches. Sortase A (SrtA) is a membrane-associated cysteine protease that catalyzes a cell wall sorting reaction by which surface proteins, including virulence factors, are anchored to the bacterial cell wall of Gram(+) bacteria. Although SrtA inhibition seems perspective among the Gram-positive pathogen-targeted antivirulence strategies, it still remains less popular than other alternatives. A decrease in virulence due to inactivation of SrtA activity has been extensively studied in Staphylococcus aureus, but it has also been demonstrated in other Gram(+) species. In this manuscript, results of past studies on the discovery of novel SrtA inhibitory compounds and evaluation of their potency were summarized and commented on. Here, we discussed the rationale behind the inhibition of SrtA, raised some concerns on the comparability of the results from different studies, and touched upon the possible resistance mechanisms as a response to implementation of such therapy in practice. The goal of this article is to encourage further studies of SrtA inhibitory compounds.

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Rapid in vivo development of resistance to daptomycin in vancomycin-resistant Enterococcus faecium due to genomic rearrangements

10.1101/2021.09.24.461763 ◽

2021 ◽

Author(s):

Sarah Mollerup ◽

Christine Elmeskov ◽

Heidi Gumpert ◽

Mette Pinholt ◽

Tobias Steen Sejersen ◽

...

Keyword(s):

Cell Wall ◽

Enterococcus Faecium ◽

Chromosomal Rearrangements ◽

Resistance Mechanisms ◽

Resistant Isolate ◽

Wall Structure ◽

Whole Genome ◽

Cyclic Lipopeptide ◽

Vancomycin Resistant

AbstractBackgroundDaptomycin is a cyclic lipopeptide used in the treatment of vancomycin-resistant Enterococcus faecium (VREfm). However, the development of daptomycin-resistant VREfm challenges the treatment of nosocomial VREfm infections. Resistance mechanisms of daptomycin are not fully understood. Here we analysed the genomic changes leading to a daptomycin-susceptible VREfm isolate becoming resistant after 40 days of daptomycin and linezolid combination therapy.MethodsThe two isogenic VREfm isolates (daptomycin-susceptible and daptomycin-resistant) were analysed using whole genome sequencing with Illumina and Nanopore.ResultsWhole genome comparative analysis identified the loss of a 46.5 kb fragment and duplication of a 29.7 kb fragment in the daptomycin-resistant isolate, with many implicated genes involved in cell wall synthesis. Two plasmids of the daptomycin-susceptible isolate were also found integrated in the chromosome of the resistant isolate. One nonsynonymous SNP in the rpoC gene was identified in the daptomycin-resistant isolate.ConclusionsDaptomycin resistance developed through chromosomal rearrangements leading to altered cell wall structure. Such novel types of resistance mechanisms can only be identified by comparing closed genomes of isogenic isolates.

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Functional Genomics Analysis of Horseweed (Conyza canadensis) with Special Reference to the Evolution of Non–Target-Site Glyphosate Resistance

Weed Science ◽

10.1614/ws-d-09-00037.1 ◽

2010 ◽

Vol 58 (2) ◽

pp. 109-117 ◽

Cited By ~ 48

Author(s):

Joshua S. Yuan ◽

Laura L. G. Abercrombie ◽

Yongwei Cao ◽

Matthew D. Halfhill ◽

Xin Zhou ◽

...

Keyword(s):

Functional Genomics ◽

Molecular Mechanisms ◽

Glyphosate Resistance ◽

Resistance Mechanisms ◽

Target Site ◽

Environmentally Benign ◽

Conyza Canadensis ◽

Target Site Resistance ◽

Weedy Species ◽

Heterologous Microarray

The evolution of glyphosate resistance in weedy species places an environmentally benign herbicide in peril. The first report of a dicot plant with evolved glyphosate resistance was horseweed, which occurred in 2001. Since then, several species have evolved glyphosate resistance and genomic information about nontarget resistance mechanisms in any of them ranges from none to little. Here, we report a study combining iGentifier transcriptome analysis, cDNA sequencing, and a heterologous microarray analysis to explore potential molecular and transcriptomic mechanisms of nontarget glyphosate resistance of horseweed. The results indicate that similar molecular mechanisms might exist for nontarget herbicide resistance across multiple resistant plants from different locations, even though resistance among these resistant plants likely evolved independently and available evidence suggests resistance has evolved at least four separate times. In addition, both the microarray and sequence analyses identified non–target-site resistance candidate genes for follow-on functional genomics analysis.

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Target and Non–target site Mechanisms Confer Resistance to Glyphosate in Canadian Accessions ofConyza canadensis

Weed Science ◽

10.1017/wsc.2017.69 ◽

2017 ◽

Vol 66 (2) ◽

pp. 234-245 ◽

Cited By ~ 8

Author(s):

Eric R. Page ◽

Christopher M. Grainger ◽

Martin Laforest ◽

Robert E. Nurse ◽

Istvan Rajcan ◽

...

Keyword(s):

Ssr Markers ◽

Resistance Mechanisms ◽

Target Site ◽

Conyza Canadensis ◽

Weed Species ◽

Target Site Resistance ◽

Selection For ◽

Simple Sequence ◽

Growing Region ◽

Selection Of

Glyphosate-resistant populations ofConyza canadensishave been spreading at a rapid rate in Ontario, Canada, since first being documented in 2010. Determining the genetic relationship among existing Ontario populations is necessary to understand the spread and selection of the resistant biotypes. The objectives of this study were to: (1) characterize the genetic variation ofC. canadensisaccessions from the province of Ontario using simple sequence repeat (SSR) markers and (2) investigate the molecular mechanism (s) conferring resistance in these accessions. Ninety-eightC. canadensisaccessions were genotyped using 8 SSR markers. Germinable accessions were challenged with glyphosate to determine their dose response, and the sequences of 5-enolpyruvylshikimate-3-phosphate synthase genes 1 and 2 were obtained. Results indicate that a majority of glyphosate-resistant accessions from Ontario possessed a proline to serine substitution at position 106, which has previously been reported to confer glyphosate resistance in other crop and weed species. Accessions possessing this substitution demonstrated notably higher levels of resistance than non–target site resistant (NTSR) accessions from within or outside the growing region and were observed to form a subpopulation genetically distinct from geographically proximate glyphosate-susceptible and NTSR accessions. Although it is unclear whether other non–target site resistance mechanisms are contributing to the levels of resistance observed in target-site resistant accessions, these results indicate that, at a minimum, selection for Pro-106-Ser has occurred in addition to selection for non–target site resistance and has significantly enhanced the levels of resistance to glyphosate inC. canadensisaccessions from Ontario.

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The Cell Envelope Stress Response of Bacillus subtilis towards Laspartomycin C

Antibiotics ◽

10.3390/antibiotics9110729 ◽

2020 ◽

Vol 9 (11) ◽

pp. 729

Author(s):

Angelika Diehl ◽

Thomas M. Wood ◽

Susanne Gebhard ◽

Nathaniel I. Martin ◽

Georg Fritz

Keyword(s):

Cell Wall ◽

Bacillus Subtilis ◽

Stress Response ◽

Cell Envelope ◽

Resistance Mechanisms ◽

Detailed Knowledge ◽

Knock Out ◽

Lipid Ii ◽

Envelope Stress ◽

The Impact

Cell wall antibiotics are important tools in our fight against Gram-positive pathogens, but many strains become increasingly resistant against existing drugs. Laspartomycin C is a novel antibiotic that targets undecaprenyl phosphate (UP), a key intermediate in the lipid II cycle of cell wall biosynthesis. While laspartomycin C has been thoroughly examined biochemically, detailed knowledge about potential resistance mechanisms in bacteria is lacking. Here, we use reporter strains to monitor the activity of central resistance modules in the Bacillus subtilis cell envelope stress response network during laspartomycin C attack and determine the impact on the resistance of these modules using knock-out strains. In contrast to the closely related UP-binding antibiotic friulimicin B, which only activates ECF σ factor-controlled stress response modules, we find that laspartomycin C additionally triggers activation of stress response systems reacting to membrane perturbation and blockage of other lipid II cycle intermediates. Interestingly, none of the studied resistance genes conferred any kind of protection against laspartomycin C. While this appears promising for therapeutic use of laspartomycin C, it raises concerns that existing cell envelope stress response networks may already be poised for spontaneous development of resistance during prolonged or repeated exposure to this new antibiotic.

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Resistance Mechanisms of Saccharomyces cerevisiae to Commercial Formulations of Glyphosate Involve DNA Damage Repair, the Cell Cycle, and the Cell Wall Structure

G3 Genes|Genome|Genetics ◽

10.1534/g3.120.401183 ◽

2020 ◽

Vol 10 (6) ◽

pp. 2043-2056

Author(s):

Apoorva Ravishankar ◽

Amaury Pupo ◽

Jennifer E. G. Gallagher

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Wall ◽

Resistance Mechanisms ◽

Mapk Signaling ◽

Fragile Sites ◽

Cell Wall Structure ◽

Wall Structure ◽

Global Changes ◽

Expression Of Genes ◽

Wide Range

The use of glyphosate-based herbicides is widespread and despite their extensive use, their effects are yet to be deciphered completely. The additives in commercial formulations of glyphosate, though labeled inert when used individually, have adverse effects when used in combination with other additives along with the active ingredient. As a species, Saccharomyces cerevisiae has a wide range of resistance to glyphosate-based herbicides. To investigate the underlying genetic differences between sensitive and resistant strains, global changes in gene expression were measured, when yeast were exposed to a glyphosate-based herbicide (GBH). Expression of genes involved in numerous pathways crucial to the cell’s functioning, such as DNA replication, MAPK signaling, meiosis, and cell wall synthesis changed. Because so many diverse pathways were affected, these strains were then subjected to in-lab-evolutions (ILE) to select mutations that confer increased resistance. Common fragile sites were found to play a role in adaptation to resistance to long-term exposure of GBHs. Copy number increased in approximately 100 genes associated with cell wall proteins, mitochondria, and sterol transport. Taking ILE and transcriptomic data into account it is evident that GBHs affect multiple biological processes in the cell. One such component is the cell wall structure which acts as a protective barrier in alleviating the stress caused by exposure to inert additives in GBHs. Sed1, a GPI-cell wall protein, plays an important role in tolerance of a GBH. Hence, a detailed study of the changes occurring at the genome and transcriptome levels is essential to better understand the effects of an environmental stressor such as a GBH, on the cell as a whole.

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Sequestration and Oxygen Radical Detoxification as Mechanisms of Paraquat Resistance

Weed Science ◽

10.1017/s0043174500080395 ◽

1994 ◽

Vol 42 (2) ◽

pp. 277-284 ◽

Cited By ~ 36

Author(s):

Jonathan J. Hart ◽

Joseph M. Di Tomaso

Keyword(s):

Active Oxygen Species ◽

Radical Scavenging ◽

Resistance Mechanisms ◽

Oxygen Radical ◽

Membrane Properties ◽

Chloroplast Envelope ◽

Cross Resistance ◽

Paraquat Resistance ◽

Plant Cell Membranes ◽

Scavenging Enzymes

Evidence in the literature has generally supported either of two paraquat resistance mechanisms: an increase in activity of oxygen radical-scavenging enzymes in resistant plants which affords protection from active oxygen species formed by paraquat; and sequestration of paraquat away from its site of action in the chloroplast. Evidence for the first model relies primarily on measurement of increased enzyme activity and cross-resistance to other oxygen radical-generating stresses in resistant plants. The sequestration model is supported by data showing decreased translocation of paraquat and absence of paraquat injury in plant systems that do not have increased levels of protective enzymes. An alteration in paraquat transport at one of several plant cell membranes could confer resistance by modifying movement of paraquat into the compartment bounded by that membrane. Properties of the plasmalemma, chloroplast envelope, and tonoplast that may be important to paraquat transport are discussed and data supporting or discounting specific membrane alterations in resistant plants are presented. Finally, the possibility that both mechanisms may work in concert is addressed.

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Evaluation of Paraquat Resistance Mechanisms in Conyza

Pesticide Biochemistry and Physiology ◽

10.1006/pest.1993.1055 ◽

1993 ◽

Vol 46 (3) ◽

pp. 236-249 ◽

Cited By ~ 30

Author(s):

M.A. Norman ◽

E.P. Fuerst ◽

R.J. Smeda ◽

K.C. Vaughn

Keyword(s):

Resistance Mechanisms ◽

Paraquat Resistance

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Reduced Vancomycin Susceptibility in Staphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

Clinical Microbiology Reviews ◽

10.1128/cmr.00042-09 ◽

2010 ◽

Vol 23 (1) ◽

pp. 99-139 ◽

Cited By ~ 541

Author(s):

Benjamin P. Howden ◽

John K. Davies ◽

Paul D. R. Johnson ◽

Timothy P. Stinear ◽

M. Lindsay Grayson

Keyword(s):

Staphylococcus Aureus ◽

Cell Wall ◽

Treatment Failure ◽

Treatment Outcomes ◽

Susceptibility Testing ◽

Point Mutations ◽

Resistance Mechanisms ◽

Wall Thickening ◽

Clinical Implications ◽

The Past

SUMMARY The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.

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