scholarly journals Sourgrass Resistance Mechanism to the Herbicide Glyphosate

2019 ◽  
Vol 37 ◽  
Author(s):  
M.S.C. MELO ◽  
L.J.F.N. ROCHA ◽  
C.A.C.G. BRUNHARO ◽  
M. NICOLAI ◽  
V.L. TORNISIELLO ◽  
...  

ABSTRACT: The knowledge on the mechanism that gives a weed resistance to a particular herbicide is essential regarding scientific, academic, and practical aspects because it determines the recommendations for prevention and management of resistance in the field. Studies on the sourgrass (Digitaria insularis) glyphosate resistance mechanism in the literature have not been conclusive. Thus, the aim of this research was to study and evaluate the putative resistance mechanisms whichgives sourgrass biotypes, the ability to survive after glyphosate application. For this, 14C-glyphosate leaf absorption and translocation were compared in the biotypes Matão (R), Campo Florido (MG), Diamantino (MT), and Iracemápolis (S) as a function of the time after its application. In addition, the possibility that the mechanism of resistance results from a mutation in the EPSPs-encoding gene was also studied. The biotypes S, R, MG, and MT absorbed similar amounts of 14C-glyphosate. The biotypes R, MG, and MT did not present differences in 14C-glyphosate translocation when compared to the biotype S. The sequencing of the EPSPs-encoding gene showed no mutation in the regions 106 and 182, which normally give resistance to glyphosate in the case of other species. No mutation in the EPSPs-encoding gene was observed. Therefore, they are not glyphosate resistance mechanisms for the evaluated biotypes.

2020 ◽  
pp. 1-12 ◽  
Author(s):  
Maxwel C Oliveira ◽  
Darci A Giacomini ◽  
Nikola Arsenijevic ◽  
Gustavo Vieira ◽  
Patrick J Tranel ◽  
...  

Abstract Failure to control Palmer amaranth with glyphosate and protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides was reported across southwestern Nebraska in 2017. The objectives of this study were to 1) confirm and 2) validate glyphosate and PPO-inhibitor (fomesafen and lactofen) resistance in 51 Palmer amaranth accessions from southwestern Nebraska using genotypic and whole-plant phenotypic assay correlations and cluster analysis, and 3) determine which agronomic practices might be influencing glyphosate resistance in Palmer amaranth accessions in that location. Based on genotypic assay, 88% of 51 accessions contained at least one individual with amplification (>2 copies) of the 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS) gene, which confers glyphosate resistance; and/or a mutation in the PPX2 gene, either ΔG210 or R128G, which endows PPO-inhibitor resistance in Palmer amaranth. Cluster analysis and high correlation (0.83) between genotypic and phenotypic assays demonstrated that EPSPS gene amplification is the main glyphosate resistance mechanism in Palmer amaranth accessions from southwestern Nebraska. In contrast, there was poor association between genotypic and phenotypic responses for PPO-inhibitor resistance, which was attributed to segregation for PPO-inhibitor resistance within these accessions and/or the methodology that was adopted herein. Genotypic assays can expedite the process of confirming known glyphosate and PPO-inhibitor resistance mechanisms in Palmer amaranth from southwestern Nebraska and other locations. Phenotypic assays are also a robust method for confirming glyphosate resistance but not necessarily PPO-inhibitor resistance in Palmer amaranth. Moreover, random forest analysis of glyphosate resistance in Palmer amaranth indicated that EPSPS gene amplification, county, and current and previous crops are the main factors influencing glyphosate resistance within that geographic area. Most glyphosate-susceptible Palmer amaranth accessions were found in a few counties in areas with high crop diversity. Results presented here confirm the spread of glyphosate resistance and PPO-inhibitor resistance in Palmer amaranth accessions from southwestern Nebraska and demonstrate that less diverse cropping systems are an important driver of herbicide resistance evolution in Palmer amaranth.


2013 ◽  
Vol 64 (9) ◽  
pp. 892 ◽  
Author(s):  
Shamsul A. Bhuiyan ◽  
Barry J. Croft ◽  
Emily C. Deomano ◽  
Rebecca S. James ◽  
Joanne K. Stringer

Resistance of sugarcane plants to smut is believed to be manifested by two mechanisms, (i) external resistance, governed by structural barrier of bud scale and/or chemical secretion from the bud, and (ii) internal resistance, regulated by interaction of plants and fungus within the plant tissue. Hot water treatments are routinely used to treat seed cane to eliminate a range of diseases including smut. It is believed that hot water treatment predisposes sugarcane plant to smut. This study was conducted to determine the resistance mechanisms of some important Australian parent clones, and their response to hot water treatment in relation to smut infection. Twenty-one clones, used regularly in the Australian sugarcane breeding program, were evaluated. Results showed that ~47% of clones had external and 33% had internal resistance mechanisms, indicating that parent clones selected for this study possessed diverse mechanism of resistance. There is a possibility some or all clones with internal resistance mechanisms could also possess external resistance mechanism. Except one highly susceptible clone (Q205) in one trial, none of the clones subject to hot water treatment became more susceptible to smut. Although some clones showed increased resistance after hot water treatment. These findings will benefit breeders in selecting parent materials in their crossing programs to develop smut-resistant cultivars.


2006 ◽  
Vol 20 (2) ◽  
pp. 282-289 ◽  
Author(s):  
Stephen B. Powles ◽  
Christopher Preston

Resistance to the herbicide glyphosate is currently known in at least eight weed species from many countries. Some populations of goosegrass from Malaysia, rigid ryegrass from Australia, and Italian ryegrass from Chile exhibit target site–based resistance to glyphosate through changes at amino acid 106 of the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene. Mutations change amino acid 106 from proline to either serine or threonine, conferring an EPSPS weakly resistant to glyphosate. The moderate level of resistance is sufficient for commercial failure of the herbicide to control these plants in the field. Conversely, a nontarget site resistance mechanism has been documented in glyphosate-resistant populations of horseweed and rigid ryegrass from the United States and Australia, respectively. In these resistant plants, there is reduced translocation of glyphosate to meristematic tissues. Both of these mechanisms are inherited as a single, nuclear gene trait. Although at present only two glyphosate-resistance mechanisms are known, it is likely that other mechanisms will become evident. The already very large and still increasing reliance on glyphosate in many parts of the world will inevitably result in more glyphosate-resistant weeds, placing the sustainability of this precious herbicide resource at risk.


Weed Science ◽  
2009 ◽  
Vol 57 (6) ◽  
pp. 567-573 ◽  
Author(s):  
Chad E. Brewer ◽  
Lawrence R. Oliver

Greenhouse studies were established in Fayetteville, AR, to investigate glyphosate resistance in Arkansas common ragweed populations. Common ragweed seed were collected from plants in Pope and Jackson counties in Arkansas. Plants grown from seed were sprayed with one of seven glyphosate rates. Populations in Pope and Jackson counties were 21-fold and 10-fold more tolerant to glyphosate, respectively, than a known susceptible population. Based on14C-glyphosate absorption and translocation studies, reduced glyphosate absorption or translocation was not the resistance mechanism in Arkansas glyphosate-resistant common ragweed. Shikimate accumulation did not differ among the known susceptible and the two resistant populations at 3 d after treatment (DAT). However, by 5 DAT, shikimate accumulation in the two resistant populations was lower than the known susceptible population. Data indicate that glyphosate-resistant common ragweed is present in at least two locations in Arkansas, and the resistance mechanism is not an insensitive target site or reduced glyphosate absorption or translocation.


2005 ◽  
Vol 54 (11) ◽  
pp. 1055-1064 ◽  
Author(s):  
Juan Ayala ◽  
Alberto Quesada ◽  
Santiago Vadillo ◽  
Jerónimo Criado ◽  
Segundo Píriz

In this study penicillin-binding proteins (PBPs) of Bacteroides fragilis and the resistance mechanisms of this micro-organism to 11 β-lactam antibiotics were analysed. The study focused on the role of PBP2Bfr and metallo-β-lactamase in the mechanism of resistance to imipenem. The mechanism of β-lactam resistance in B. fragilis was strain dependent. The gene encoding the orthologue of Escherichia coli PBP3 gene (pbpBBfr, which encodes the protein PBP2Bfr) was sequenced in five of the eight strains studied, along with the ccrA (cfiA) gene in strain 119, and their implications for resistance were examined. Differences were found in the amino-acid sequence of PBP2Bfr in strains AK-2 and 119, and the production of β-lactamases indicated that these differences may be involved in the mechanism of resistance to imipenem. In vitro binding competition assays with membrane extracts using imipenem indicated that the PBP that bound imipenem with the highest affinity was PBP2Bfr, and that increased affinity in strain 7160 may be responsible for the moderate susceptibility of this strain to imipenem. In the same way, the importance of the chromosomal class A β-lactamase CepA in the resistance mechanism of the B. fragilis strains NCTC 9344, 7160, 2013E, AK-4, 0423 and R-212 was studied. In these strains this is the principal resistance mechanism to antimicrobial agents studied other than imipenem.


Agronomy ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 884
Author(s):  
Vhuthu Ndou ◽  
Petrus Jacobus Pieterse ◽  
Dirk Jacobus Brand ◽  
Alvera Vorster ◽  
Amandrie Louw ◽  
...  

In 2003, a glyphosate-resistant plantago (Plantago lanceolata L.) population located in the Robertson district of South Africa was subjected to different glyphosate dosages and the highest dosage (7200 g a.e. ha−1) gave no acceptable levels of control. Here we reconfirm resistance and investigate the mechanism of glyphosate resistance. Dose-response curves indicated that the glyphosate dosage rate causing 50% survival (LD50) for the resistant (R) biotype is 43 times greater than for the susceptible (S) biotype, i.e., 43-fold resistant to glyphosate. Investigation into the molecular mechanism of plantago showed shikimate accumulation of the R biotype was lower than that of the S biotype. The reported 31P and 13C nuclear magnetic resonance (NMR) spectra show rapid glyphosate translocation into the young untreated leaves of the S biotype. No glyphosate translocation was observed in the R biotype. A point mutation in the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene, resulting in an amino acid substitution was also observed, indicating two unique glyphosate resistance mechanisms within the R biotype. The rapid evolution of glyphosate-resistant weeds threatens the usage of the world’s most important herbicide (glyphosate), which is essential in world food production and further limits grower options for weed control. New weed management strategies will be necessary to combat plantago R biotypes.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shixing Liu ◽  
Renchi Fang ◽  
Ying Zhang ◽  
Lijiang Chen ◽  
Na Huang ◽  
...  

Abstract Background The emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains. Results This study showed that the mechanisms of carbapenem resistance in this study are: 1. Generating carbapenemase (7 of 19); 2. The production of AmpC or ESBLs combined with decreased expression of out membrane protein (12 of 19). hsp60 sequence analysis suggested 10 of 19 the strains belong to colistin hetero-resistant clusters and the mechanism of colistin resistance is increasing expression of acrA in the efflux pump AcrAB-TolC alone (18 of 19) or accompanied by a decrease of affinity between colistin and outer membrane caused by the modification of lipid A (14 of 19). Moreover, an ECC strain co-harboring plasmid-mediated mcr-4.3 and blaNDM-1 has been found. Conclusions This study suggested that there is no overlap between the resistance mechanism of co-resistant ECC strains to carbapenem and colistin. However, the emergence of strain co-harboring plasmid-mediated resistance genes indicated that ECC is a potential carrier for the horizontal spread of carbapenems and colistin resistance.


mSystems ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Johannes Cairns ◽  
Katariina Koskinen ◽  
Reetta Penttinen ◽  
Tommi Patinen ◽  
Anna Hartikainen ◽  
...  

ABSTRACTMobile genetic elements such as conjugative plasmids are responsible for antibiotic resistance phenotypes in many bacterial pathogens. The ability to conjugate, the presence of antibiotics, and ecological interactions all have a notable role in the persistence of plasmids in bacterial populations. Here, we set out to investigate the contribution of these factors when the conjugation network was disturbed by a plasmid-dependent bacteriophage. Phage alone effectively caused the population to lose plasmids, thus rendering them susceptible to antibiotics. Leakiness of the antibiotic resistance mechanism allowing Black Queen evolution (i.e. a “race to the bottom”) was a more significant factor than the antibiotic concentration (lethal vs sublethal) in determining plasmid prevalence. Interestingly, plasmid loss was also prevented by protozoan predation. These results show that outcomes of attempts to resensitize bacterial communities by disrupting the conjugation network are highly dependent on ecological factors and resistance mechanisms.IMPORTANCEBacterial antibiotic resistance is often a part of mobile genetic elements that move from one bacterium to another. By interfering with the horizontal movement and the maintenance of these elements, it is possible to remove the resistance from the population. Here, we show that a so-called plasmid-dependent bacteriophage causes the initially resistant bacterial population to become susceptible to antibiotics. However, this effect is efficiently countered when the system also contains a predator that feeds on bacteria. Moreover, when the environment contains antibiotics, the survival of resistance is dependent on the resistance mechanism. When bacteria can help their contemporaries to degrade antibiotics, resistance is maintained by only a fraction of the community. On the other hand, when bacteria cannot help others, then all bacteria remain resistant. The concentration of the antibiotic played a less notable role than the antibiotic used. This report shows that the survival of antibiotic resistance in bacterial communities represents a complex process where many factors present in real-life systems define whether or not resistance is actually lost.


2010 ◽  
Vol 77 (3) ◽  
pp. 786-793 ◽  
Author(s):  
Jitender Mehla ◽  
S. K. Sood

ABSTRACTA better understanding of the antimicrobial peptide (AMP) resistance mechanisms of bacteria will facilitate the design of effective and potent AMPs. Therefore, to understand resistance mechanisms and forin vitroassessment, variants ofEnterococcus faecalisthat are resistant to different doses of the fungal AMP alamethicin (Almr) were selected and characterized. The resistance developed was dose dependent, as both doses of alamethicin and degrees of resistance were colinear. The formation of bacterial cell aggregates observed in resistant cells may be the prime mechanism of resistance because overall, a smaller cell surface in aggregated cells is exposed to AMPs. Increased rigidity of the membranes of Almrvariants, because of their altered fatty acids, was correlated with limited membrane penetration by alamethicin. Thus, resistance developed against alamethicin was an adaptation of the bacterial cells through changes in their morphological features and physiological activity and the composition of membrane phospholipids. The Almrvariants showed cross-resistance to pediocin, which indicated that resistance developed against both AMPs may share a mechanism, i.e., an alteration in the cell membrane. High percentages of colorimetric response by both AMPs against polydiacetylene/lipid biomimetic membranes of Almrvariants confirmed that altered phospholipid and fatty acid compositions were responsible for acquisition of resistance. So far, this is the only report of quantification of resistance and cross-resistance using anin vitrocolorimetric approach. Our results imply that a single AMP or AMP analog may be effective against bacterial strains having a common mechanism of resistance. Therefore, an understanding of resistance would contribute to the development of a single efficient, potent AMP against resistant strains that share a mechanism of resistance.


2022 ◽  
pp. 1-7
Author(s):  
Dal-Hoe Koo ◽  
Rajendran Sathishraj ◽  
Bernd Friebe ◽  
Bikram S. Gill

In agriculture, various chemicals are used to control the weeds. Out of which, glyphosate is an important herbicide invariably used in the cultivation of glyphosate-resistant crops to control weeds. Overuse of glyphosate results in the evolution of glyphosate-resistant weeds. Evolution of glyphosate resistance (GR) in <i>Amaranthus palmeri</i> (AP) is a serious concern in the USA. Investigation of the mechanism of GR in AP identified different resistance mechanisms of which <i>5-enolpyruvylshikimate-3-phosphate synthase</i> (<i>EPSPS</i>) gene amplification is predominant. Molecular analysis of GR AP identified the presence of a 5- to &#x3e;160-fold increase in copies of the <i>EPSPS</i> gene than in a glyphosate-susceptible (GS) population. This increased copy number of the <i>EPSPS</i> gene increased the genome size ranging from 3.5 to 11.8%, depending on the copy number compared to the genome size of GS AP. FISH analysis using a 399-kb <i>EPSPS</i> cassette derived from bacterial artificial chromosomes (BACs) as probes identified that amplified <i>EPSPS</i> copies in GR AP exist in extrachromosomal circular DNA (eccDNA) in addition to the native copy in the chromosome. The <i>EPSPS</i> gene-containing eccDNA having a size of ∼400 kb is termed <i>EPSPS</i>-eccDNA and showed somatic mosacism in size and copy number. <i>EPSPS</i>-eccDNA has a genetic mechanism to tether randomly to mitotic or meiotic chromosomes during cell division or gamete formation and is inherited to daughter cells or progeny generating copy number variation. These eccDNAs are stable genetic elements that can replicate and exist independently. The genomic characterization of the <i>EPSPS</i> locus, along with the flanking regions, identified the presence of a complex array of repeats and mobile genetic elements. The cytogenomics approach in understanding the biology of <i>EPSPS</i>-eccDNA sheds light on various characteristics of <i>EPSPS</i>-eccDNA that favor GR in AP.


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