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Molecular Basis of Resistance to Herbicides Inhibiting Acetolactate Synthase in Two Rigid Ryegrass (Lolium rigidum) Populations from Australia

Published online by Cambridge University Press:  20 January 2017

Shiv S. Kaundun*
Affiliation:
Syngenta, Jealott's Hill International Research Centre, Bracknell, Berkshire RG42 6EY, United Kingdom
Richard P. Dale
Affiliation:
Syngenta, Jealott's Hill International Research Centre, Bracknell, Berkshire RG42 6EY, United Kingdom
Géraldine C. Bailly
Affiliation:
Syngenta, Jealott's Hill International Research Centre, Bracknell, Berkshire RG42 6EY, United Kingdom Imperial College London, Faculty of Life Science, Ascot, Berkshire SL6 7PY, United Kingdom
*
Corresponding author's E-mail: deepak.kaundun@syngenta.com

Abstract

Acetolactate Synthase- (ALS) inhibiting herbicides are important components for the control of ryegrass species infesting cereal-cropping systems worldwide. Although resistance to ALS herbicides in ryegrasses has evolved more than 25 yr ago, few studies have been dedicated to elucidate the molecular mechanisms involved. To this end, we have investigated the molecular basis of chlorsulfuron, sulfometuron-methyl, and imazapyr resistance in AUS5 and AUS23, two ryegrass populations from Australia. Comparison between whole-plant herbicide assays and DNA sequencing results showed that resistance to the nonmetabolizable herbicide sulfometuron-methyl was associated with four different proline mutations at ALS codon position 197 (P197) in AUS23. In addition to three P197 amino acid changes impacting on the efficacies of the two sulfonylurea herbicides, the tryptophan to leucine target-site mutation at ALS codon position 574 (W574L) was present in AUS5, conferring resistance to both sulfometuron-methyl and imazapyr. The samples were also characterized by non target-site-based resistance impacting on the metabolizable herbicide chlorsulfuron only. Interestingly, compound mutant heterozygotes threonine/serine at ALS position 197, and plants with double mutations at positions 197 and 574 were detected, thus reflecting the ability of this outcrossing species to accumulate mutant alleles. Whole-plant dose-response assays conducted on predetermined wild-type and mutant genotypes originating from the same populations allowed for a more precise estimation of the dominant and very high levels of resistance associated with the proline to serine target-site mutation at ALS codon position 197 (P197S) and W574L mutations. The two highly efficient polymerase chain reaction- (PCR) based derived cleaved amplified polymorphic sequence (dCAPS) markers developed here will allow for quick confirmation of 197 and 574 ALS target-site resistance in ryegrass species field samples and also contribute to identify populations characterized by other likely resistance mechanisms in this important weed species.

Type
Physiology, Chemistry, and Biochemistry
Copyright
Copyright © Weed Science Society of America 

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References

Literature Cited

Christopher, J. T., Powles, S. B., and Holtum, J.A.M. 1992. Resistance to acetolactate synthase-inhibiting herbicides in annual ryegrass (Lolium rigidum) involves at least two mechanisms. Plant Physiol. 100:19091913.Google Scholar
Dayhoff, M. O., Schwartz, R. M., and Orcutt, B. C. 1978. A model of evolutionary change in proteins. Pages 345352 in Dayhoff, M. O., ed. Atlas of Protein Sequence and Structure. Washington, D.C. National Biomedical Research Foundation.Google Scholar
Delye, C., Boucansaud, K., Pernin, F., and Le Corre, V. 2009. Variation in the gene encoding acetolactate-synthase in Lolium species and proactive detection of mutant, herbicide-resistant alleles. Weed Res. 49:326336.Google Scholar
Delye, C., Pernin, F., and Michel, S. 2011. ‘Universal’ PCR assays detecting mutations in acetyl-coenzyme A carboxylase or acetolactate synthase that endow herbicide resistance in grass weeds. Weed Res. 51:353362.CrossRefGoogle Scholar
Heap, I. M. 2011. International Survey of Herbicide-Resistant Weeds. http://www.weedscience.com. Accessed: November 10, 2011.Google Scholar
Kaundun, S. S., Dale, R., and Lycett, A. 2006. Molecular basis of acetolactate synthase (ALS) inhibitor resistance in two rye grass (Lolium rigidum) populations. Page 102 in Proceedings of the Weed Science Society of America. Publisher: New York Proc. Weed Sci. Soc. am. [Abstract].Google Scholar
Kaundun, S. S. and Windass, J. D. 2006. Derived cleaved amplified polymorphic sequence, a simple method to detect a key point mutation conferring acetyl CoA carboxylase inhibitor herbicide resistance in grass weeds. Weed Res. 46:3439.Google Scholar
Laplante, J., Rajcan, I., and Tardif, F. J. 2009. Multiple allelic forms of acetohydroxyacid synthase are responsible for herbicide resistance in Setaria viridis . Theor. Appl. Genet. 119:577585.Google Scholar
Massa, D., Krenz, B., and Gerhards, R. 2011. Target-site resistance to ALS-inhibiting herbicides in Apera spica-venti populations is conferred by documented and previously unknown mutations. Weed Res. 51:294303.Google Scholar
Moss, S. R., Marshall, R., Hull, R., and Alarcon-Reverte, R. 2011. Current status of herbicide-resistant weeds in the United Kingdom. Pages 110 in Proceedings of the Aspects of Applied Biology. Crop Protection in Southern Britain. Warwick, UK Association of Applied Biologists.Google Scholar
Neff, M. M., Neff, J. D., Chory, J., and Pepper, A. E. 1998. dCAPS, a simple technique for the genetic analysis of single nucleotide polymorphisms: experimental applications in Arabidposis thaliana genetics. Plant J. 14:387392.Google Scholar
Neff, M. M., Turk, E., and Kalishman, M. 2002. Web-based primer design for single nucleotide polymorphism analysis. Trends Genet. 18:613615.Google Scholar
Owen, M. J., Walsh, M. J., Llewellyn, R. S., and Powles, S. B. 2007. Widespread occurrence of multiple herbicide resistance in Western Australian annual ryegrass (Lolium rigidum) populations. Aust. J. Agric. Res. 58:711718.Google Scholar
Park, K. W. and Mallory-Smith, C. A. 2004. Physiological and molecular basis for ALS inhibitor resistance in Bromus tectorum biotypes. Weed Res. 44:7177.Google Scholar
Powles, S. and Yu, Q. 2010. Evolution in action: plants reistant to herbicides. Annu. Rev. Plant Biol. 61:317–47.Google Scholar
R Development Core Team. 2009. R: A language and environment for statistical computing. Vienna, Austria R Foundation for Statistical Computing. http://www.R-project.org. Accessed: October 5, 2009.Google Scholar
Ray, T. B. 1984. Site of action of chlorsulfuron: inhibition of valine and isoleucine biosynthesis in plants. Plant Physiol. 75:827831.CrossRefGoogle ScholarPubMed
Ritz, C. and Streibig, J. C. 2005. Bioassay analysis using R. J. Stat. Softw. 12: issue 5.Google Scholar
Sibony, M., Michel, A., Haas, H. U., Rubin, B., and Hurle, K. 2001. Sulfometuron-resistant Amaranthus retroflexus: cross-resistance and molecular basis for resistance to acetolactate synthase-inhibiting herbicides. Weed Res. 41:509522.Google Scholar
Tan, M. K., Preston, C., and Wang, G. X. 2007. Molecular basis of multiple resistance to ACCase-inhibiting and ALS-inhibiting herbicides in Lolium rigidum . Weed Res. 47:534541.Google Scholar
Tranel, P. J. and Wright, T. R. 2002. Resistance of weeds to ALS-inhibiting herbicides: what have we learned? Weed Sci. 50:700712.Google Scholar
Yu, Q., Han, H., and Powles, S. B. 2008. Mutations of the ALS gene endowing resistance to ALS-inhibiting herbicides in Lolium rigidum populations. Pest Manag. Sci. 64:12291236.Google Scholar
Yu, Q., Han, H., Vila-Aiub, M., and Powles, S. B. 2010. AHAS herbicide resistance endowing mutations: effect on AHAS functionality and plant growth. J. Exp. Bot. 61:39253934.Google Scholar