Congruences modulo prime powers of Hecke eigenvalues in level 11

We continue the study of strong, weak, and $dc$-weak eigenforms introduced by Chen, Kiming, and Wiese. We completely determine all systems of Hecke eigenvalues of level $1$ modulo $128$, showing there are finitely many. This extends results of Hatada and can be considered as evidence for the more general conjecture formulated by the author together with Kiming and Wiese on finiteness of systems of Hecke eigenvalues modulo prime powers at any fixed level. We also discuss the finiteness of systems of Hecke eigenvalues of level $1$ modulo $9$, reducing the question to the finiteness of a single eigenvalue. Furthermore, we answer the question of comparing weak and $dc$-weak eigenforms and provide the first known examples of non-weak $dc$-weak eigenforms.Comment: 28 pages; Minor revisio

Metabolic Pathway of Topramezone in Multiple-Resistant Waterhemp (Amaranthus tuberculatus) Differs From Naturally Tolerant Maize

Waterhemp [Amaranthus tuberculatus (Moq.) Sauer] is a problematic dicot weed in maize, soybean, and cotton production in the United States. Waterhemp has evolved resistance to several commercial herbicides that inhibit the 4-hydroxyphenylpyruvate-dioxygenase (HPPD) enzyme in sensitive dicots, and research to date has shown that HPPD-inhibitor resistance is conferred by rapid oxidative metabolism of the parent compound in resistant populations. Mesotrione and tembotrione (both triketones) have been used exclusively to study HPPD-inhibitor resistance mechanisms in waterhemp and a related species, A. palmeri (S. Wats.), but the commercial HPPD inhibitor topramezone (a pyrazolone) has not been investigated from a mechanistic standpoint despite numerous reports of cross-resistance in the field and greenhouse. The first objective of our research was to determine if two multiple herbicide-resistant (MHR) waterhemp populations (named NEB and SIR) metabolize topramezone more rapidly than two HPPD inhibitor-sensitive waterhemp populations (named SEN and ACR). Our second objective was to determine if initial topramezone metabolite(s) detected in MHR waterhemp are qualitatively different than those formed in maize. An excised leaf assay and whole-plant study investigated initial rates of topramezone metabolism (<24 h) and identified topramezone metabolites at 48 hours after treatment (HAT), respectively, in the four waterhemp populations and maize. Results indicated both MHR waterhemp populations metabolized more topramezone than the sensitive (SEN) population at 6 HAT, while only the SIR population metabolized more topramezone than SEN at 24 HAT. Maize metabolized more topramezone than any waterhemp population at each time point examined. LC-MS analysis of topramezone metabolites at 48 HAT showed maize primarily formed desmethyl and benzoic acid metabolites, as expected based on published reports, whereas SIR formed two putative hydroxylated metabolites. Subsequent LC-MS/MS analyses identified both hydroxytopramezone metabolites in SIR as different hydroxylation products of the isoxazole ring, which were also present in maize 48 HAT but at very low levels. These results indicate that SIR initially metabolizes and detoxifies topramezone in a different manner than tolerant maize

Broad Resistance to ACCase Inhibiting Herbicides in a Ryegrass Population Is Due Only to a Cysteine to Arginine Mutation in the Target Enzyme

BACKGROUND: The design of sustainable weed management strategies requires a good understanding of the mechanisms by which weeds evolve resistance to herbicides. Here we have conducted a study on the mechanism of resistance to ACCase inhibiting herbicides in a Lolium multiflorum population (RG3) from the UK. METHODOLOGY/PRINCIPAL FINDINGS: Analysis of plant phenotypes and genotypes showed that all the RG3 plants (72%) that contained the cysteine to arginine mutation at ACCase codon position 2088 were resistant to ACCase inhibiting herbicides. Whole plant dose response tests on predetermined wild and mutant 2088 genotypes from RG3 and a standard sensitive population indicated that the C2088R mutation is the only factor conferring resistance to all ten ACCase herbicides tested. The associated resistance indices ranged from 13 for clethodim to over 358 for diclofop-methyl. Clethodim, the most potent herbicide was significantly affected even when applied on small mutant plants at the peri-emergence and one leaf stages. CONCLUSION/SIGNIFICANCE: This study establishes the clear and unambiguous importance of the C2088R target site mutation in conferring broad resistance to ten commonly used ACCase inhibiting herbicides. It also demonstrates that low levels "creeping", multigenic, non target site resistance, is not always selected before single gene target site resistance appears in grass weed populations subjected to herbicide selection pressure

A novel W1999S mutation and non-target site resistance impact on acetyl-CoA carboxylase inhibiting herbicides to varying degrees in a UK Lolium multiflorum population.

Acetyl-CoA carboxylase (ACCase) inhibiting herbicides are important products for the post-emergence control of grass weed species in small grain cereal crops. However, the appearance of resistance to ACCase herbicides over time has resulted in limited options for effective weed control of key species such as Lolium spp. In this study, we have used an integrated biological and molecular biology approach to investigate the mechanism of resistance to ACCase herbicides in a Lolium multiflorum Lam. from the UK (UK21).The study revealed a novel tryptophan to serine mutation at ACCase codon position 1999 impacting on ACCase inhibiting herbicides to varying degrees. The W1999S mutation confers dominant resistance to pinoxaden and partially recessive resistance to cycloxydim and sethoxydim. On the other hand, plants containing the W1999S mutation were sensitive to clethodim and tepraloxydim. Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden. The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance

dCAPS procedures for the detection of the wild type isoleucine and mutant threonine amino acid residues at ACCase codon position 1781: (4a) <i>Nsi</i>I restricted (134 bp) correspond to the I1781 allele and unrestricted fragments (165 bp) correspond to either T1781 or L1781 alleles.

<p>(4b) <i>Nde</i>I restricted fragments (132 bp) correspond to the mutant threonine allele while the undigested band (169 bp) corresponds to either the wild type isoleucine or leucine alleles. Heterozygous plants show one each of the restricted and unrestricted PCR fragments in the two assays.</p

Correlation between cycloxydim phenotypes and combined genotypes at ACCase codon positions 1781 and 2027.

<p>Correlation between cycloxydim phenotypes and combined genotypes at ACCase codon positions 1781 and 2027.</p

CAPS procedure for the detection of a thymine to cysteine change (C2088R mutation) at nucleotide position 6262 in <i>Lolium</i> spp.

<p>The <i>Hha</i> I digested fragment (126 bp) correspond to the resistant R2088 allele and the <i>Hha</i> 1 undigested fragment (161 bp) correspond to the C2088 allele. Heterozygous plants display both the 126 bp and 161 resistant and sensitive alleles respectively. Lanes 1 and 10: DNA ladder, lanes 2, 3 and 4: homozygous mutant RR2088, lanes 4, 5, 6: heterozygous CR2088 plants, lanes 7, 8, 9: homozygous wild CC2088 plants.</p

Cycloxydim whole plant dose response tests on four plant groups.

<p>Homozygous wild type STD1-II1781 from the standard sensitive population; homozygous wild type BG2-II1781; heterozygous mutant type BG2-IT1781 and heterozygous mutant type BG2-IL1781 from population BG2.</p

Herbicide rates used in whole plant dose response assays.

<p>CC2088-STD1: wild type homozygous 2088 genotype from standard sensitive population.</p><p>CC2088-RG3: wild type homozygous 2088 genotype from population RG3.</p><p>RR2088-RG3: mutant homozygous 2088 genotype from population RG3.</p

Pinoxaden whole plant dose response tests on four plant groups.

<p>Homozygous wild type STD1-II1781 from the standard sensitive population; homozygous wild type BG2-II1781; heterozygous mutant type BG2-IT1781 and heterozygous mutant type BG2-IL1781 from population BG2.</p