Populations genetics and the evolution of herbicide resistance in weeds

De nombreux facteurs, incluant les mutations, la sélection, l'hérédité, le système de reproduction et le flux génique sont importants dans révolution de la résistance aux herbicides chez les mauvaises herbes. Les mutations spontanées seraient la principale source de variation génétique pouvant causer l'évolution de la résistance dans une région géographique où la résistance n'a pas été détectée auparavant. En dépit de la fréquence des mutations qui est probablement très faible, la probabilité qu'apparaisse au moins un mutant résistant dans une population sensible peut être élevée chez les espèces de mauvaises herbes qui ont une fécondité élevée et des populations importantes. Des traitements subséquents répétés, avec des herbicides ayant un même mode d'action, pourraient conduire à l'évolution rapide de populations composées en prédominance d'individus résistants. Les mutations de résistance héritées de façon dominante se propagent significativement plus rapidement que les mutations récessives chez les populations se reproduisant au hasard, mais à peu près au même rythme chez les espèces auto-fertiles. Le flux génique issu de la dispersion du pollen ou des graines des populations de mauvaises herbes résistantes peut procurer une source d'allèles de résistance à des champs sensibles adjacents ou avoisinants. Les modèles mathématiques indiquent que la pression de sélection imposée par un herbicide et la fréquence initiale du phénotype résistant influence très fortement le taux d'évolution de la résistance. Les modèles prédisent que les stratégies les plus efficaces pour gérer la résistance sont de réduire l'intensité de sélection par l'herbicide et de limiter la migration de graines résistantes aux herbicides.Numerous factors, including mutation, selection, inheritance, mating System, and gene flow are important in the evolution of herbicide resistance in weeds. Spontaneous gene mutation is believed to be the main source of genetic variation for resistance evolution in a geographic region in which resistance has not been detected previously. Despite mutation frequencies that are probably very low, the probability of occurrence of at least a single resistant mutant in a susceptible population may be high for weed species with high fecundities and large population sizes. Subsequent repeated treatments with herbicides having the same mode of action could lead to the rapid evolution of predominantly resistant populations. Rare dominantly inherited resistance mutations spread significantly more rapidly than recessive mutations in random mating populations, but at roughly the same rate in highly self-fertilizing species. Gene flow, through the movement of pollen or seed from resistant weed populations, may provide a source of resistance alleles to adjacent or nearby susceptible fields. Mathematical models indicate that the strength of selection imposed by a herbicide and the initial frequency of the resistant phenotype most strongly influence the rate of resistance evolution. The models predict that the most effective strategies to manage resistance are to reduce the intensity of selection by herbicide and to limit the migration of herbicide-resistant seed

Auxinic herbicides, mechanisms of action, and weed resistance: A look into recent plant science advances

Auxin governs dynamic cellular processes involved at several stages of plant growth and development. In this review, we discuss the mechanisms employed by auxin in light of recent scientific advances, with a focus on synthetic auxins as herbicides and synthetic auxin resistance mechanisms. Two auxin receptors were reported. The plasma membrane receptor ABP1 (Auxin Binding Protein 1) alters the structure and arrangement of actin filaments and microtubules, leading to plant epinasty and reducing peroxisomes and mitochondria mobility in the cell environment. The second auxin receptor is the gene transcription pathway regulated by the SCFTir/AFB ubiquitination complex, which destroys transcription repressor proteins that interrupt Auxin Response Factor (ARF) activation. As a result mRNA related with Abscisic Acid (ABA) and ethylene are transcribed, producing high quantities of theses hormones. Their associated action leads to high production of Reactive Oxygen Species (ROS), leading to tissue and plant death. Recently, another ubiquitination pathway which is described as a new auxin signaling route is the F-box protein S-Phase Kinase-Associated Protein 2A (SKP2A). It is active in cell division regulation and there is evidence that auxin herbicides can deregulate the SKP2A pathway, which leads to severe defects in plant development. In this discussion, we propose that SFCSKP2A auxin binding site alteration could be a new auxinic herbicide resistance mechanism, a concept which may contribute to the current progress in plant biology in its quest to clarify the many questions that still surround auxin herbicide mechanisms of action and the mechanisms of weed resistance