Target and Nontarget Resistance Mechanisms Induce Annual Bluegrass (<i>Poa annua</i>) Resistance to Atrazine, Amicarbazone, and Diuron

Svyantek, Andrej; Aldahir, Phillipe; Chen, Shu; Flessner, Michael L.; McCullough, Patrick E.; Sidhu, Sudeep S.; McElroy, J. Scott

doi:10.1614/wt-d-15-00173.1

Cited by 32 publications

(31 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Decreased absorption is not a common NTSR mechanism, but has been reported with resistance of common sunflower (Helianthus annuus) to imazethapyr and chlorimuron (71), prickly lettuce (Lactuca serriola) to 2,4-D, annual bluegrass (Poa annua) to atrazine (72), and L. multiflorum and S. halepense to glyphosate (73,74). No differences were found in cuticular wax amount per unit area of leaf surface between two biotypes of L. multiflorum with a three-fold difference in glyphosate susceptibility and reduced absorption in the less sensitive biotype (75).…”

Section: Reduced Absorptionmentioning

confidence: 99%

Mechanisms of evolved herbicide resistance

Gaines

Duke

Morran

et al. 2020

Journal of Biological Chemistry

395

493

View full text Add to dashboard Cite

The widely successful use of synthetic herbicides over the past 70 years has imposed strong and widespread selection pressure, leading to the evolution of herbicide resistance in hundreds of weed species. Both target-site resistance (TSR) and non-target-site resistance (NTSR) mechanisms have evolved to most herbicide classes. TSR often involves mutations in genes encoding the protein targets of herbicides, affecting the binding of the herbicide either at or near catalytic domains or in regions affecting access to them. Most of these mutations are non-synonymous single-nucleotide polymorphisms, but polymorphisms in more than one codon or entire codon deletions have also evolved. Some herbicides bind multiple proteins, making TSR mechanisms more difficult to evolve. Increased amounts of protein target, by increased gene expression or by gene duplication, is an important, albeit less common, TSR mechanism. NTSR mechanisms include reduced absorption or translocation and increased sequestration or metabolic degradation. The mechanisms that can contribute to NTSR are complex and often involve genes that are members of large gene families. For example, enzymes involved in herbicide metabolism–based resistances include cytochromes P450, glutathione-S-transferases, glucosyl and other transferases, aryl acylamidase, and others. Both TSR and NTSR mechanisms can combine at the individual level to produce higher resistance levels. The vast array of herbicide-resistance mechanisms for generalist (NTSR) and specialist (TSR and some NTSR) adaptations that have evolved over a few decades illustrate the evolutionary resilience of weed populations to extreme selection pressures. These evolutionary processes drive herbicide and herbicide-resistant crop development and resistance management strategies.

show abstract

Section: Reduced Absorptionmentioning

confidence: 99%

Mechanisms of evolved herbicide resistance

Gaines

Duke

Morran

et al. 2020

Journal of Biological Chemistry

395

493

View full text Add to dashboard Cite

show abstract

“…For example, red amaranth ( Amaranthus cruenatus ) and smooth pigweed ( Amaranthus hybridus ) populations that are resistant to atrazine showed negative cross‐resistance to bentazone and pyridate (De Prado et al ). However, triazine‐resistant redroot pigweed ( Amaranthus retroflexus ) (Arntzen et al ) and annual bluegrass ( Poa annua ) (Svyantek et al ) were equally as susceptible to diuron as the triazine‐susceptible populations. In the current study, the two triazine‐resistant populations that were investigated (P17 and P18) were equally sensitive to diuron as the two susceptible populations (S1 and S2), which is consistent with the mutation (Ser‐264‐Gly) (Fig.…”

Section: Discussionmentioning

confidence: 99%

Identification of a target‐site mutation conferring resistance to triazine herbicides in oriental mustard (Sisymbrium orientale L.) from Australia

Dang

Malone

Boutsalis

et al. 2017

Weed Biology and Management

View full text Add to dashboard Cite

In southern Australia, oriental mustard (Sisymbrium orientale) has been controlled successfully by triazine herbicides for several decades. The screening of 40 populations that were collected from the southern grain belt of Australia during 2010 and 2013 for resistance to six different herbicides (glyphosate, diflufenican, imazamox, chlorsulfuron, atrazine and 2,4‐dichlorophenoxyacetic acid) identified two oriental mustard populations as highly resistant to atrazine. Compared to the known oriental mustard‐susceptible populations (S1 and S2), these two resistant populations (P17 and P18) from near Horsham, Victoria, Australia, were 311‐ and 315‐fold resistant to atrazine, as determined by a comparison of the LD50 values. However, there was no resistance to diuron detected in these populations. Sequencing of the chloroplast psbA gene identified a missense mutation of serine 264 to glycine in both herbicide‐resistant oriental mustard populations, which is known to confer high‐level atrazine resistance in other species.

show abstract

“…Este cambio se ha encontrado en los biotipos resistentes de Amaranthus hybridus, Solanum nigrum, Brassica napus, Brassica campestris, Capsella bursa-pastoris, Chenopodium album, Raphanus raphanistrum, Poa annua y S. vulgaris. El cambio ha sido en el aminoácido 264 que es parte del nicho de acople del herbicida en la proteína D1, el aminoácido serina fue reemplazo por glicina (Devine y Shukla 2000, Trebst 2008, Hirschberg y McIntosh 1983, Shane Friesen y Powles 2007, Svyantek et al 2015. Las malezas resistentes no han tenido cambios en la absorción, translocación ni degradación del herbicida, cambios que también pueden conferir resistencia (Radosevich y DeVilliers 1976).…”

Section: Mecanismos De Resistencia a Los Herbicidas Queunclassified

Modo de Acción y Resistencia de los Herbicidas que Interfieren en el Fotosistema II de la Fotosíntesis

Pitty

2018

Ceiba

View full text Add to dashboard Cite

Unos herbicidas matan a las plantas deteniendo el transporte de electrones en el fotosistema II. Ellos compiten con la plastoquinona (PQ), un transportador de electrones, por el sitio de acople en la proteína D1 del fotosistema II. Cuando el herbicida se acopla al nicho de la PQ, detiene el flujo de electrones porque el herbicida no puede aceptar ni donar electrones como la PQ. Esto causa que la clorofila no pueda transferir la energía que absorbe o recibe de los pigmentos accesorios; al quedar excitada forma clorofila triplete que causa la peroxidación de los lípidos y la muerte de las células. Además, la clorofila triplete reacciona con oxígeno molecular (O2) y forma oxígeno singlete o singulete (1O2), una forma reactiva de oxígeno que daña los lípidos de las membranas celulares. Luego se destruye la clorofila y los carotenoides, y se pierde la semipermeabilidad e integridad de las membranas celulares. Las membranas destruidas dejan escapar el contenido celular a los espacios intercelulares y las células mueren. Más de 70 especies han desarrollado resistencia a algunos de estos herbicidas y el mecanismo más común es una modificación en el genoma del sitio de acople del herbicida en el fotosistema II. En unas especies cambió el aminoácido 264 en la proteína D1, el aminoácido serina fue reemplazado por glicina o treonina; en otras cambió valina por isoleucina en la posición 219; en la posición 251 alanina por valina y en la posición 266 asparagina por treonina. Estos cambios reducen la afinidad del herbicida por el sitio de acople y la eficiencia del transporte de electrones, reduciendo la fotosintesis. Debido a que el cloroplasto tiene su propio genoma, esta resistencia se hereda de la madre. Unos biotipos han desarrollado resistencia porque tienen un metabolismo acelerado y detoxifican el herbicida más rápido que los susceptibles. La detoxificación es causada por una actividad alta de la enzima glutatión transferasa que conjuga el herbicida con el glutatión.

show abstract

Target and Nontarget Resistance Mechanisms Induce Annual Bluegrass (Poa annua) Resistance to Atrazine, Amicarbazone, and Diuron

Cited by 32 publications

References 39 publications

Mechanisms of evolved herbicide resistance

Mechanisms of evolved herbicide resistance

Identification of a target‐site mutation conferring resistance to triazine herbicides in oriental mustard (Sisymbrium orientale L.) from Australia

Modo de Acción y Resistencia de los Herbicidas que Interfieren en el Fotosistema II de la Fotosíntesis

Contact Info

Product

Resources

About