Evolution of Herbicide Resistance in Senecio vulgaris: Variation in Susceptibility to Simazine Between and Within Populations

Holliday, R.; Putwain, P. D.

doi:10.2307/2402655

Cited by 41 publications

(18 citation statements)

References 22 publications

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“…In addition to variation at major resistance genes, continuous and heritable variation in susceptibility to low herbicide rates has been documented in weed populations (see Holliday and Putwain 1980;Jasieniuk et al, 1996;Patzoldt et al, 2002). While the genetic basis for this variation is not reported, continuous variation usually indicates polygenic control at numerous minor loci.…”

Section: Introductionmentioning

confidence: 99%

High survival frequencies at low herbicide use rates in populations of Lolium rigidum result in rapid evolution of herbicide resistance

2005

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The frequency of phenotypic resistance to herbicides in previously untreated weed populations and the herbicide dose applied to these populations are key determinants of the dynamics of selection for resistance. In total, 31 Lolium rigidum populations were collected from sites with no previous history of exposure to herbicides and where there was little probability of gene flow from adjacent resistant populations. The mean survival frequency across all 31 populations following two applications of commercial rates (375 g ha À1 ) of the acetyl-coenzyme A carboxylase (ACCase) inhibiting herbicide, diclofop-methyl was 0.43%. Survivors from five of these populations were grown to maturity and seed was collected. Dose-response experiments compared population level resistance to diclofop-methyl in these selected lines with their original parent populations. A single cycle of herbicide selection significantly increased resistance in all populations (LD 50 R:S ratios ranged from 2.8 to 23.2), confirming the inheritance and genetic basis of phenotypic resistance. In vitro assays of ACCase inhibition by diclofop acid indicated that resistance was due to a non-target-site mechanism. Following selection with diclofop-methyl, the five L. rigidum populations exhibited diverse patterns of crossresistance to ACCase and ALS-inhibiting herbicides, suggesting that different genes or gene combinations were responsible for resistance. The relevance of these results to the management of herbicide resistance are discussed. Heredity (2005) 95, 485-492.

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Section: Introductionmentioning

confidence: 99%

High survival frequencies at low herbicide use rates in populations of Lolium rigidum result in rapid evolution of herbicide resistance

2005

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“…Differences in genotype explain why some weeds develop herbicide resistance when selection pressure is provided by frequent use of triazine herbicides (Holliday and Putwain 1980). Within the genus Pinus, some species demonstrate a greater tolerance to herbicides than others (Kosinski andHolt 1985, Wood et al 1993).…”

Section: Genotypementioning

confidence: 99%

Results from sixPinus taedanursery trials with the herbicide pendimethalin in the USA

South

Hill

2009

Southern Forests: a Journal of Forest Science

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“…In this respect they are clearly on target. For example, there are yet no direct genetic data to support that the resistance shown in figure 3(C) is quantitatively inherited, although there are data for quantitative inheritance in a similar case in the mild resistance to triazines in Senecio vulgaris (Holliday and Putwain, 1980), a species where monogenic target site resistance is also known. There is also some genetic evidence for quantitatively inherited incremental increases in some fungicide resistances (see Brent et al, 1990;Holloman et al, 1990;DeWaard, 1992), insecticides (see Mouches et al, 1986;Field et al, 1988), herbicides (Wang et al, 1991) and anti-cancer drugs (see Schimke, 1984).…”

Section: Selecting For/delaying Quantitatively Inherited Resistancementioning

confidence: 99%

A revolving dose strategy to delay the evolution of both quantitative vs major monogene resistances to pesticides and drugs

Gardner¹,

Gressel²,

Mangel³

1998

International Journal of Pest Management

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A revolving dose strategy to delay the evolution of both quantitative vs major monogene resistances to pesticides and drugs (Abs tract. The evolution of pesticide and drug resistance presents a daunting problem as the pests often evolve resistance after a short time. Debate once focused on whether resistance stems primarily from single major gene sources or sequential accumulation of quantitative traits. Such debates became moot, as examples of both are known, even within the same species and population. The type of resistance has important implications for determining the dosages that will delay the appearance of resistant populations. Successive high doses of a toxin (i.e. those well above the LD99) can only select for monogenic resistance, while the weaker selection pressure of low (near lethal) doses can also result in an incremental increase in quantitative changes leading to increasingly higher levels of resistance. We propose and use a model to mathematically test whether a revolving rotation of a series of low doses periodically alternated with a higher dose could delay the evolution of resistance longer than by applying a constant dose (either low or high) in every treatment. We suggest this dosage rotation strategy for situations in which crops and alternative pesticides or drugs cannot be rotated, and suggest that it be used in conjunction with other methods of control (biocontrol, IPM) to further delay resistance. We model the evolution of resistance under truncation selection (more typical in the laboratory), as well as under a smooth selection regime that is more likely to describe selection in the field where pests develop more asynchronously, and application is less uniform. In addition, we consider the level of population control imposed by the toxin, since, for economic and health reasons, both the size of the pest population as well as the frequency of resistant pests must be considered. We also examine how the degree of dominance of the major resistance gene and changes in heritability with repeated episodes of selection affect the success of dosage rotation compared with constant doses. Modelled dosage rotations could delay resistance and suppress pest populations longer and require less pesticide (or drug) than successive constant doses. Constant doses may suffice to delay resistance over the short run if heritability is low, but revolving doses are essential over longer periods. The modelled results seem worthy of field validation, as they predict a longer resistance-free period at the lowest possible doses.

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Evolution of Herbicide Resistance in Senecio vulgaris: Variation in Susceptibility to Simazine Between and Within Populations

Cited by 41 publications

References 22 publications

High survival frequencies at low herbicide use rates in populations of Lolium rigidum result in rapid evolution of herbicide resistance

High survival frequencies at low herbicide use rates in populations of Lolium rigidum result in rapid evolution of herbicide resistance

Results from sixPinus taedanursery trials with the herbicide pendimethalin in the USA

A revolving dose strategy to delay the evolution of both quantitative vs major monogene resistances to pesticides and drugs

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