Distribution of PPX2 Mutations Conferring PPO-Inhibitor Resistance in Palmer Amaranth Populations of Tennessee

2018 ◽  
Vol 32 (5) ◽  
pp. 592-596 ◽  
Author(s):  
J. Drake Copeland ◽  
Darci A. Giacomini ◽  
Patrick J. Tranel ◽  
Garret B. Montgomery ◽  
Lawrence E. Steckel

AbstractProtoporphyrinogen IX oxidase (PPO)–inhibiting herbicides (WSSA Group 14) have been used in agronomic row crops for over 50 yr. Broadleaf weeds, including glyphosate-resistant Palmer amaranth, have been controlled by this herbicide site of action PRE and POST. Recently, Palmer amaranth populations were reported resistant to PPO inhibitors in 2011 in Arkansas, in 2015 in Tennessee, and in 2016 in Illinois. Historically, the mechanism for this resistance involves the deletion of a glycine at position 210 (ΔG210) in a PPO enzyme encoded by the PPX2 gene; however, the ΔG210 deletion did not explain all PPO inhibitor–resistant Palmer amaranth in Tennessee populations. Recently, two new mutations within PPX2 (R128G, R128M) that confer resistance to PPO inhibitors were identified in Palmer amaranth. Therefore, research is needed to document the presence and distribution of the three known mutations that confer PPO inhibitor resistance in Tennessee. In 2017, a survey was conducted in 18 fields with Palmer amaranth to determine whether resistance existed and the prevalence of each known mutation in each field. Fomesafen was applied at 265 g ai ha–1 to Palmer amaranth infestations within each field to select for resistant weeds for later analysis. Where resistance was described (70% of surviving plants), the ΔG210 mutation was detected in 47% of resistant plants. The R128G mutation accounted for 42% of resistance, similar to the frequency of the ΔG210 mutation. The R128M mutation was less frequent than the other two mutations, accounting for only 10% of the resistance. All mutations detected in this study were heterozygous. Additionally, no more than one of the three PPX2 mutations were detected in an individual surviving plant. Similar to previous research, about 70% of PPO resistance was accounted for by these three known mutations, leaving about 30% of resistance not characterized in Tennessee populations. Survivors not showing the three known PPO mutations suggest that other resistance mechanisms are present.

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.


Weed Science ◽  
2017 ◽  
Vol 66 (2) ◽  
pp. 149-158 ◽  
Author(s):  
Vijay K. Varanasi ◽  
Chad Brabham ◽  
Jason K. Norsworthy ◽  
Haozhen Nie ◽  
Bryan G. Young ◽  
...  

Palmer amaranth is one of the most problematic weeds in the midsouthern United States, and the evolution of resistance to protoporphyrinogen oxidase (PPO) inhibitors in biotypes already resistant to glyphosate and acetolactate synthase (ALS) inhibitors is a major cause of concern to soybean and cotton growers in these states. A late-season weed-escape survey was conducted in the major row crop–producing counties (29 counties) to determine the severity of PPO-inhibitor resistance in Arkansas. A total of 227 Palmer amaranth accessions were sprayed with fomesafen at 395 g ha−1to identify putative resistant plants. A TaqMan qPCR assay was used to confirm the presence of the ΔG210 codon deletion or the R128G/M (homologous to R98 mutation in common ragweed) target-site resistance mechanisms in thePPX2gene. Out of the 227 accessions screened, 44 were completely controlled with fomesafen, and 16 had only one or two severely injured plants (≥98% mortality) when compared with the 1986 susceptible check (100% mortality). The remaining 167 accessions were genotypically screened, and 82 (49%) accessions were found to harbor the ΔG210 deletion in thePPX2gene. The R128G was observed in 47 (28%) out of the 167 accessions screened. The mutation R128M, on the other hand was rare, found in only three accessions. About 13% of the accessions were segregating for both the ΔG210 and R128G mutations. Sixteen percent of the tested accessions had mortality ratings <90% and did not test positive for the ΔG210 or the R128G/M resistance mechanisms, indicating that a novel target or non–target site resistance mechanism is likely. Overall, PPO inhibitor–resistant Palmer amaranth is widespread in Arkansas, and the ΔG210 resistance mechanism is especially dominant in the northeast corridor, while the R128G mutation is more prevalent in counties near Memphis, TN.


Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2968
Author(s):  
Anuhya Kommalapati ◽  
Sri Harsha Tella ◽  
Mitesh Borad ◽  
Milind Javle ◽  
Amit Mahipal

Fibroblast Growth Factor receptor (FGFR) pathway aberrations have been implicated in approximately 7% of the malignancies. As our knowledge of FGFR aberrations in cancer continues to evolve, FGFR inhibitors emerged as potential targeted therapeutic agents. The promising results of pemigatinib and infigratinib in advanced unresectable cholangiocarcinoma harboring FGFR2 fusions or rearrangement, and erdafitinib in metastatic urothelial carcinoma with FGFR2 and FGFR3 genetic aberrations, lead to their accelerated approval by the United States (USA) FDA. Along with these agents, many phase II/III clinical trials are currently evaluating the use of derazantinib, infigratinib, and futibatinib either alone or in combination with immunotherapy. Despite the encouraging results seen with FGFR inhibitors, resistance mechanisms and side effect profile may limit their clinical utility. A better understanding of the unique FGFR-inhibitor-related toxicities would invariably help us in the prevention and effective management of FGFR-inhibitor-induced adverse events thereby enhancing their clinical benefit. Herein, we summarized the physiology of FGF/FGFR signaling and briefly discussed the possible mechanisms that could lead to FGFR inhibitor resistance and side effects. In addition, we proposed treatment guidelines for the management of FGFR-inhibitor-associated toxicities. This work would invariably help practicing oncologists to effectively manage the unique toxicities of FGFR inhibitors.


1981 ◽  
Vol 34 (4) ◽  
pp. 737 ◽  
Author(s):  
E Horn ◽  
MR Snow

The title compound has been prepared from Re(CO)5Br by a bromide-abstraction reaction with silver fluoride. It completes the series of known halide clusters of the type [Re(CO)3X]4 (where X = halide). The crystals are tetragonal, space group 14, with a 11.716(5), c 8.988(3) �, and Z 2. The structure was refined by full-matrix least-squares to an R value of 0.027 for 1380 observed reflections. The molecules are cubane-type clusters of Re(CO)3 groups at one set of corners interpenetrated with fluorine atoms at the other set. The clusters exhibit the molecular symmetry 43m. Each of the fluorine atoms is involved in μ3 type bridging with the rhenium atoms at an average bonding distance of 2.200(5) �. The clusters are held together by hydrogen bonding of fluoride to water molecules.


2021 ◽  
pp. canres.1208.2021
Author(s):  
Jorge Gómez Tejeda Zañudo ◽  
Pingping Mao ◽  
Clara Alcon ◽  
Kailey Kowalski ◽  
Gabriela N Johnson ◽  
...  

Genetics ◽  
1982 ◽  
Vol 102 (2) ◽  
pp. 139-147
Author(s):  
Michael J Hynes

ABSTRACT A mutant producing very high levels of the acetamidase enzyme encoded by the amdS gene has been isolated in a strain containing the amdA7 mutation, which itself causes high levels of this enzyme. Genetic analysis has shown that this mutation, designated amdI66, is adjacent to the amdS gene and is cis-dominant in its effect. The amdI66 mutation has little effect on amdS expression when present in strains not containing the amdA7 mutation. Two other amdA mutations investigated also interact with the amdI66 mutation to result in high acetamidase levels. No interaction between amdI66 and any of the other putative regulatory genes affecting amdS expression has been observed. The amdI66 mutation has been located by fine structure mapping at the extreme end of the controlling region, which has previously been defined by genetic mapping (Hynes 1979). Analysis of this region has been extended by mapping new mutations resulting in loss of amdS expression. One of these defines the most extreme site capable of mutation to loss of gene function found so far.


Weed Science ◽  
1981 ◽  
Vol 29 (5) ◽  
pp. 571-577 ◽  
Author(s):  
Lynn M. Kitchen ◽  
William W. Witt ◽  
Charles E. Rieck

The effect of glyphosate [N-(phosphonomethyl) glycine] on barley (Hordeum vulgareL.) and corn (Zea maysL.) shoot δ-aminolevulinic acid (ALA) production was examined by monitoring ALA content in the tissue and measuring incorporation of14C precursors into ALA and chlorophylla. Barley shoot ALA content was significantly decreased by 1 mM glyphosate after 9, 11, and 15 h of illumination. ALA production by treated barley shoots was 30 nmoles•g fresh weight-1•h-1at each interval tested, compared with 75 to 120 nmoles•g fresh weight-1•h-1for the control. In corn shoots, ALA content was reduced 32, 45, and 58% by 0.1, 1.0, and 10.0 mM glyphosate, respectively, after 12 h illumination. Incorporation studies with14C-glutamate,14C-α-ketoglutarate, and14C-glycine into ALA showed a 77, 92, and 91% inhibition, respectively, in barley shoots treated with 1 mM glyphosate. Incorporation of14C-ALA into chlorophyllawas not affected by 1 mM glyphosate. Thus, the site of action of glyphosate may involve two enzyme pathways:one controlling the conversion of α-ketoglutarate to ALA, and the other controlling the condensation of glycine with succinyl CoA to form ALA and carbon dioxide. Inhibition of ALA synthesis blocks synthesis of chlorophyll, as well as all other porphyrin ring compounds found in higher plants. Thus, inhibition of ALA synthesis may be an integral component of the herbicidal mode of action of glyphosate.


Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2054
Author(s):  
Elizabeth K. Lee ◽  
Ursula A. Matulonis

The use of PARP inhibitors (PARPi) is growing widely as FDA approvals have shifted its use from the recurrence setting to the frontline setting. In parallel, the population developing PARPi resistance is increasing. Here we review the role of PARP, DNA damage repair, and synthetic lethality. We discuss mechanisms of resistance to PARP inhibition and how this informs on novel combinations to re-sensitize cancer cells to PARPi.


Weed Science ◽  
2020 ◽  
Vol 68 (3) ◽  
pp. 253-259
Author(s):  
Yajun Peng ◽  
Lang Pan ◽  
Ducai Liu ◽  
Xiaomei Cheng ◽  
Guolan Ma ◽  
...  

AbstractChinese sprangletop [Leptochloa chinensis (L.) Nees] is one grass weed severely affecting rice (Oryza sativa L.) growth in paddies in China. Cyhalofop-butyl is the main herbicide used to control grass weeds in Chinese paddy fields, especially for controlling L. chinensis; however, L. chinensis has evolved resistance to cyhalofop-butyl due to continuous and extensive application. To investigate cyhalofop-butyl resistance levels and mechanisms in L. chinensis in some of the Chinese rice areas, 66 field populations were collected and treated with cyhalofop-butyl. Of these tested populations, 10 showed a high level of resistance to cyhalofop-butyl; the 50% effective dose ranged within 108.4 to 1,443.5 g ai ha−1 with resistance index values of 9.1 to 121.8 when compared with the susceptible population. Acetyl-coenzyme A carboxylase genes (ACCase) of susceptible and all 10 resistant populations were amplified and sequenced. Among them, Ile-1781-Leu, Trp-2027-Cys, Trp-2027-Ser, and Ile-2041-Asn mutations were found in five resistant populations. No known resistance-related mutations were found in the other five resistant populations, indicating that resistance to cyhalofop-butyl in these populations was likely to be endowed by non–target site resistance mechanisms. Notably, the Ile-1781-Leu and Trp-2027-Cys substitutions have previously been reported, but this is the first report of Trp-2027-Ser and Ile-2041-Asn mutations in L. chinensis. Furthermore, three derived cleaved amplified polymorphic sequence methods were developed to rapidly detect these mutations in L. chinensis.


2021 ◽  
Vol 92 ◽  
pp. 102137
Author(s):  
E. Kun ◽  
Y.T.M. Tsang ◽  
C.W. Ng ◽  
D.M. Gershenson ◽  
K.K. Wong

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