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Managing the risks of herbicide resistance in wild oat

Published online by Cambridge University Press:  20 January 2017

Graeme Cavan ,
John Cussans  and
Stephen Moss
Graeme Cavan
Affiliation:
Department of Crop and Weed Science, IACR-Rothamsted, Harpenden, Hertfordshire AL5 2JQ, U.K.
John Cussans
Affiliation:
Department of Crop and Weed Science, IACR-Rothamsted, Harpenden, Hertfordshire AL5 2JQ, U.K.
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Abstract

A single dominant mutation conferring resistance to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides was incorporated into a quantitative model for the population development of wild oat. The model was used to predict the times required to develop field resistance in a number of different scenarios. Field resistance was defined as a threshold of four plants m−2 surviving herbicide treatment, and in most scenarios, a very large proportion of these plants were resistant. The model predicts that plow cultivation could delay the development of resistance relative to tine cultivation. With an initial seed bank of 100 seeds m−2 and annual use of AOPP/CHD herbicides, which kill 90% of susceptible but no resistant plants, field resistance develops in 15 yr with annual tine cultivation 10 cm deep but only after 23 yr with annual plowing 20 cm deep. The model predicts that herbicide rotation can dramatically increase the times required for field resistance to develop in a tine cultivation system. With annual use of AOPP/CHD herbicides, field resistance develops in 15 yr, whereas using alternative modes of action 1 in 2 yr delays field resistance to 28 yr. The model predicts that resistance can be delayed for at least 66 yr if three herbicides, each with a different mode of action, are rotated and each herbicide causes 90% mortality. The model predictions on the number of years required for field resistance to develop are not highly sensitive to the initial density of the seed bank (range modeled = 102 to 104), the mutation rate for resistance (10−4 to 10−7 per generation), the rate of outcrossing (0.1 to 100%) or the herbicide kill rate (80 to 95%).

Keywords

Wild oat, Avena fatua L. AVEFAaryloxyphenoxypropionate herbicidecyclohexanedione herbicideModelweed life cycleACCase inhibitorevolutioncultural controlrotationAVEFA
Type
Weed Management
Information
Weed Science , Volume 49 , Issue 2 , April 2001 , pp. 236 - 240
Copyright
Copyright © Weed Science Society of America 

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References

Literature Cited

Bourgeois, L. and Morrison, I. N. 1997. Mapping risk areas for resistance to ACCase inhibitor herbicides in Manitoba. Can. J. Plant Sci. 77:173–179.CrossRefGoogle Scholar
Cocker, K. M., Coleman, J.O.D., Blair, A. M., Clarke, J. H., and Moss, S. R. 2000. Biochemical mechanisms of cross-resistance to aryloxyphenox-ypropionate and cyclohexanedione herbicides in populations of Avena spp. (wild-oats). Weed Res. 40:323–334.CrossRefGoogle Scholar
Cousens, R. D. 1986. The use of population models in the study of the economics of weed control. Pages 269–276 In Proceedings of the European Weed Research Society Symposium on Economic Weed Control, Stuttgart, Germany. Wageningen, The Netherlands: European Weed Research Society.Google Scholar
Derrick, R. A. 1933. Natural crossing with wild-oats (Avena fatua). Sci. Agric. 13:458–459.Google Scholar
Gardner, S. N., Gressel, J., and Mangel, M. 1998. A revolving dose strategy to delay the evolution of both quantitative vs. major monogene resistances to pesticides and drugs. Int. J. Pest Manag. 44:161–180.Google Scholar
Gonzalez-Andujar, J. L. and Perry, J. N. 1995. Models for the herbicidal control of the seed bank of Avena sterilis—the effects of spatial and temporal heterogeneity and of dispersal. J. Appl. Ecol. 32:578–587.Google Scholar
Heap, I. 1997. The occurrence of herbicide-resistant weeds worldwide. Pestic. Sci. 51:235–243; see also http://www.weedscience.com.3.0.CO;2-N>CrossRefGoogle Scholar
Kibite, S., Harker, K. N., and Brown, P. D. 1995. Inheritance of resistance to diclofop-methyl and fenoxaprop-p-ethyl in two Avena sativa × Avena fatua populations. Can. J. Plant Sci. 75:81–85.Google Scholar
Maneechote, C., Preston, C., and Powles, S. B. 1997. A diclofop-methylresistant Avena sterilis biotype with an herbicide-resistant acetyl-coenzyme A carboxylase and enhanced metabolism of diclofop-methyl. Pestic. Sci. 49:105–114.Google Scholar
Moss, S. R. 1990. The seed cycle of Alopecurus myosuroides in winter cereals: a quantitative analysis. Pages 27–35 In Proceedings of the European Weed Research Society Symposium on Integrated Weed Management in Cereals. Helsinki, Finland: European Weed Research Society.Google Scholar
Murray, B. G. 1996. Inheritance and Pollen-Mediated Gene Flow of Acetyl-CoA Carboxylase Inhibitor Resistance in Wild Oat (Avena fatua). . University of Manitoba, Winnipeg. 133 p.Google Scholar
Murray, B. G., Brule-Babel, A. L., and Morrison, I. N. 1996. Two distinct alleles encode for acetyl-CoA carboxylase inhibitor resistance in wild oat (Avena fatua). Weed Sci. 44:476–481.Google Scholar
Murray, B. G., Morrison, I. N., and Brule-Babel, A. L. 1995. Inheritance of acetyl-CoA carboxylase inhibitor resistance in wild oat (Avena fatua). Weed Sci. 43:233–238.CrossRefGoogle Scholar
Seefeldt, S. S., Fuerst, E. P., Gealy, D. R., Shukla, A., Irzyk, G. P., and Devine, M. D. 1996. Mechanisms of resistance to diclofop of two wild oat (Avena fatua) biotypes from the Willamette Valley of Oregon. Weed Sci. 44:776–781.Google Scholar
Seefeldt, S. S., Hoffman, D. L., Gealy, D. R., and Fuerst, E. P. 1998. Inheritance of diclofop resistance in wild oat (Avena fatua L.) biotypes from the Willamette Valley of Oregon. Weed Sci. 46:170–175.CrossRefGoogle Scholar
Thurston, J. M. and Phillippson, A. 1976. Distribution. Pages 19–64 In Jones, D. P., ed. Wild Oats in World Agriculture. London: Agricultural Research Council.Google Scholar
Wilson, B. J. 1980. The influence of reduced cultivations and direct drilling on the long-term decline of a population of Avena fatua L. in spring barley. Weed Res. 21:23–28.CrossRefGoogle Scholar
Wilson, B. J. 1985. Effect of seed age and cultivation on seedling emergence and seed decline of Avena fatua L. in winter barley. Weed Res. 25:213–219.CrossRefGoogle Scholar
Wilson, B. J., Cousens, R., and Cussans, G. W. 1984. Exercises in modelling populations of Wild oat to aid strategic planning for the long term control of this weed in cereals. Pages 287–294 In Proceedings of the 7th International Symposium on Weed Biology, Ecology and Systematics, Paris. Paris: COLUMA.Google Scholar