Hostname: page-component-cd9895bd7-lnqnp Total loading time: 0 Render date: 2024-12-22T19:37:59.889Z Has data issue: false hasContentIssue false
  • English
  • Français

Inheritance of Acetyl-CoA Carboxylase Inhibitor Resistance in Wild Oat (Avena fatua)

Published online by Cambridge University Press:  12 June 2017

Bruce G. Murray ,
Ian N. Morrison  and
Anita L. Brûlé-Babel
Bruce G. Murray
Affiliation:
Dep. Plant Sci., Univ. Manitoba, Winnipeg, Manitoba, Canada, R3T 2N2
Ian N. Morrison
Affiliation:
Dep. Plant Sci., Univ. Manitoba, Winnipeg, Manitoba, Canada, R3T 2N2
Anita L. Brûlé-Babel
Affiliation:
Dep. Plant Sci., Univ. Manitoba, Winnipeg, Manitoba, Canada, R3T 2N2
Get access Rights & Permissions [Opens in a new window]

Abstract

Resistance to fenoxaprop-P and other aryloxyphenoxypropionate and cyclohexanedione herbicides in the wild oat population, UM1, is controlled by a single, partially dominant, nuclear gene. In arriving at this conclusion, parents, F1 hybrids, and F2 plants derived from reciprocal crosses between UM1 and a susceptible wild oat line, UM5, were treated with fenoxaprop-P over a wide range of dosages. Based on these experiments, a dosage of 400 g ai ha−1 fenoxaprop-P was selected to discriminate between three response types. At this dosage, susceptible plants were killed and resistant plants were unaffected, whereas plants characterized as intermediate in response were injured but recovered. Treated F2 plants segregated in a 1:2:1 (R, I, S) ratio, indicative of single nuclear gene inheritance. This was confirmed by selfing F2 plants and screening several F3 families. Families derived from intermediate F2 plants segregated for the three characteristic response types, whereas those derived from resistant F2 plants were uniformly resistant. Chisquare analysis indicated the F2 segregation ratios fit those expected for a single partially dominant nuclear gene system. In addition, F2 populations from both crosses were screened with a mixture of fenoxaprop-Pand sethoxydim. The dosages of both herbicides (150 g ai ha−1 fenoxaprop-P and 100 g ha−1 sethoxydim) were sufficient to control only susceptible plants. Treated F2 populations segregated in a 3:1 (R:S) pattern, thereby confirming that resistance to the two chemically unrelated herbicides results from the same gene alteration.

Keywords

Fenoxaprop-P [R-2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid, ethyl estersethoxydim, [2-[1-(ethoxyimino)butyl]-5-[2-(ethylthio)-propyl]-3-hydroxy-2-cyclohexen-1-one]wild oat, Avena fatua L. #3AVEFAFenoxaprop-p-ethylaryloxyphenoxypropionatecyclohexanedioneACCaseherbicide resistanceweed geneticsAVEFA
Type
Weed Biology and Ecology
Information
Weed Science , Volume 43 , Issue 2 , June 1995 , pp. 233 - 238
Copyright
Copyright © 1995 by the Weed Science Society of America 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

LITERATURE CITED

1. Barr, A. R., Mansooji, A. M., Holtum, J.A.M., and Powles, S. B. 1992. The inheritance of herbicide resistance in Avena sterilis ssp ludoviciana, biotype SAS 1. Page 70–72 in Proc. 1st International Weed Control Congress, Melborne, Australia.Google Scholar
2. Betts, K. J., Ehlke, N. J., Wyse, D. L., Gronwald, J. W., and Somers, D. A. 1992. Mechanism of inheritance of diclofop resistance in Italian ryegrass (Lolium multiflorum). Weed Sci. 40:184–189.Google Scholar
3. Brain, P., and Cousens, R. 1989. An equation to describe dose responses where there is stimulation of growth at low doses. Weed Res. 29:93–96.CrossRefGoogle Scholar
4. Chauvel, B. 1991 Polymorphisme génétique et sélection de la résistance aux urées substituées chez Alopecurus myosuroides Huds. Ph.D. thesis. Université de Paris-sud Centre d'Orsay.Google Scholar
5. Duesing, J. 1983. Genetic analysis of herbicide resistance. Proc. North Central Weed Control Conf. 38:143–147.Google Scholar
6. Gressel, J. and Segel, . 1978. The paucity of plants evolving genetic resistance to herbicides: possible reasons and implications. J. Theor. Biol. 75:349–371.Google Scholar
7. Gressel, J. and Segel, L. A. 1990. Modelling the effectiveness of herbicide rotations and mixtures as strategies to delay or preclude resistance. Weed Technol 4:186–198.Google Scholar
8. Heap, I. M., Murray, B. G., Loeppky, H. A., and Morrison, I. N. 1993. Resistance to aryloxyphenoxypropionate and cyclohexanedione herbicides in wild oat (Avena fatua). Weed Sci. 41:232–238.CrossRefGoogle Scholar
9. Jasieniuk, M., Brûlé-Babel, A. L., and Morrison, I. N. 1995. The evolution and genetics of herbicide resistance in agricultural weeds. Rev. Weed Sci. in press.CrossRefGoogle Scholar
10. Jasieniuk, M. A., Brûlé-Babel, A. L., and Morrison, I. N. 1994. Inheritance of trifluralin resistance in green foxtail (Setaria viridis). Weed Sci. 42:123–127.CrossRefGoogle Scholar
11. Machado, V. S. 1982. Inheritance and breeding potential of triazine tolerance and resistance in plants. Pages 257–273 in LeBaron, H. M. and Gressel, J., eds. Herbicide Resistance in Plants. J. Wiley & Sons.Google Scholar
12. Mallory-Smith, C. A., Thill, D. C., Dial, M. J., and Zemetra, R. S. 1990. Inheritance of sulfonylurea herbicide resistance in Lactuca spp. Weed Technol. 4:787–790.CrossRefGoogle Scholar
13. Maxwell, B. D., Roush, M. L., and Radosevich, S. R. 1990. Predicting the evolution and dynamics of herbicide resistance in weed populations. Weed Technol. 4:2–13.Google Scholar
14. Steele, R.G.D. and Torrie, J. H. 1980. Pages 477–492 in Napier, C. and Maisel, J. W., eds. Principles and Procedures of Statistics, a Biometrical Approach. McGraw-Hill.Google Scholar
15. Streibig, J. C. 1980. Models for curve-fitting herbicide dose response data. Acta. Agriculturae Scandinavica. 30:59–64.Google Scholar
16. Strickberger, M. W. 1976. Pages 140–164 in Genetics. MacMillan Co., Inc., New York.Google Scholar