Thiophanate‐methyl and carbendazim resistance in Fusicoccum amygdali , the causal agent of constriction canker of peach and almond

International audienceIn light of growing environmental concerns, surveys of fungicide resistance are needed to ensure efficient control of fungi and avoid unnecessary treatments. Investigations of fungicide resistance in Fusicoccum amygdali are scarce despite the economic impacts of this pathogen in peach and almond orchards. Thiophanate-methyl has been registered for more than 20 years to control F. amygdali but no resistance has been reported to date. This propesticide is metabolized by fungi into carbendazim, a β-tubulin inhibitor. Sensitivity to carbendazim of nine populations of F. amygdali from French orchards was assessed using germination bioassays. Also, resistance levels of 63 strains isolated from four populations were evaluated using mycelial growth assays. The underlying mechanism of resistance was investigated by sequencing the β-tubulin gene, the molecular target of thiophanate-methyl, in a set of isolates with different levels of sensitivity to carbendazim. Cross-resistance to thiophanate-methyl and to another β-tubulin inhibitor, diethofencarb, was also assessed in carbendazim-sensitive and -resistant strains. Isolates highly resistant to carbendazim were found in one of the nine orchards studied. Sequencing showed that resistant phenotypes carry a mutation in the β-tubulin gene leading to E198K substitution. Positive cross-resistance to thiophanate-methyl was confirmed and no negative cross-resistance to diethofencarb was identified in the phenotyped isolates, which were all resistant to this active substance. To our knowledge, this is the first report of resistance to thiophanate-methyl in F. amygdali. The high level of resistance of isolates sampled in one population is of concern, although the limited geographical scope of resistance suggests its recent emergence

A high diversity of mechanisms endows ALS-inhibiting herbicide resistance in the invasive common ragweed (Ambrosia artemisiifolia L.)

International audienceAbstract Ambrosia artemisiifolia L. (common ragweed) is a globally invasive, allergenic, troublesome arable weed. ALS-inhibiting herbicides are broadly used in Europe to control ragweed in agricultural fields. Recently, ineffective treatments were reported in France. Target site resistance (TSR), the only resistance mechanism described so far for ragweed, was sought using high-throughput genotyping-by-sequencing in 213 field populations randomly sampled based on ragweed presence. Additionally, non-target site resistance (NTSR) was sought and its prevalence compared with that of TSR in 43 additional field populations where ALS inhibitor failure was reported, using herbicide sensitivity bioassay coupled with ALS gene Sanger sequencing. Resistance was identified in 46 populations and multiple, independent resistance evolution demonstrated across France. We revealed an unsuspected diversity of ALS alleles underlying resistance (9 amino-acid substitutions involved in TSR detected across 24 populations). Remarkably, NTSR was ragweed major type of resistance to ALS inhibitors. NTSR was present in 70.5% of the resistant plants and 74.1% of the fields harbouring resistance. A variety of NTSR mechanisms endowing different resistance patterns evolved across populations. Our study provides novel data on ragweed resistance to herbicides, and emphasises that local resistance management is as important as mitigating gene flow from populations where resistance has arisen

Assessment of the Dominance Level of the R81T Target Resistance to Two Neonicotinoid Insecticides in[i] Myzus persicae[/i] (Hemiptera: Aphididae).

International audienceMyzus persicae (Sulzer, 1776), a major crop pest worldwide, displays insecticide resistance to most molecules. The R81T substitution on the β1 subunit of nicotinic receptors of acetylcholine (nAChR) confers target site resistance to neonicotinoids and is widespread in aphid populations colonizing peach tree orchards in Southern Europe. But the impact of this resistance in the field, as well as ways to optimize its management, depends largely on the dominance level of the R81T mutation. In this study, we measured by in vitro assays the response of R81T mutation to two neonicotinoids (imidacloprid and thiacloprid) in 23 M. persicae clones with different resistance genotypes in order to assess the dominance status of this allele. In this study, all homozygous clones for the R81T mutation (genotype 81(TT)) showed a much higher level of resistance to both active substances than other clones. The heterozygous clones 81(RT) displayed a slightly higher level of resistance than wild homozygous, though resistance phenotypes against both neonicotinoids in these two genotypes were overlapping. A great variation of resistance level was found within these two latter clones' categories. The dominance level of insecticide resistance (DLC) strongly suggested that the mutant allele 81T is semirecessive (the wild 81R allele being rather dominant) for both insecticide molecules under test. Mean DLC values were 0.316 for imidacloprid and 0.351 for thiacloprid. Cross-resistance was shown between imidacloprid and thiacloprid. This partial recessivity is valuable information to broaden the knowledge on neonicotinoid resistance, a prerequisite for devising adapted management strategies against insecticide-resistant populations of M. persicae

La résistance aux insecticides chez le puceron vert du pêcher: Étude des allèles de résistance aux insecticides chez le puceron vert du pêcher (Myzus persicae) et de leur dispersion spatio-temporelle dans diverses cultures

Le puceron vert du pêcher (Myzus persicae) est un insecte polyphage, capable de coloniser plus de 400 espèces végétales sauvages ou cultivées dont le pêcher, le colza, la pomme de terre et la betterave. Il occasionne des dégâts directs qui peuvent diminuer les récoltes et les rendre impropres à la commercialisation.Mais, surtout, il peut transmettre de nombreux virus sur diverses cultures agricoles. Des phénomènes de résistance aux insecticides ont été clairement identifiés. Un enjeu important pour contrôler le puceron vert du pêcher (Myzus persicae) de manière plus efficace et plus respectueuse de l’environnement est de comprendre comment les résistances peuvent se propager