INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HORSEWEED (Conyza canadensis) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase

MUTATION: PROLINE 197 to SERINE

Horseweed (Conyza canadensis) is a dicot plant in the asteraceae family. A single amino acid substitution from Proline 197 to Serine has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Horseweed

Chemical Family	Example Herbicide	Resistance Level
Imidazolinones	Imazethapyr	Susceptible
Pyrimidinyl benzoates	Bispyribac-Na	Resistant > 10 fold
Sulfonylureas	Chlorsulfuron	Resistant > 10 fold
Triazolopyrimidine - Type 1	Chloransulam-methyl	Resistant > 10 fold
Triazolinones	Flucarbazone-Na	Not Determined

REFERENCES

Zheng, D. M. ; Kruger, G. R. ; Singh, S. ; Davis, V. M. ; Tranel, P. J. ; Weller, S. C. ; Johnson, W. G.. 2011. Cross-resistance of horseweed (Conyza canadensis) populations with three different ALS mutations. Pest Management Science 67 : 1486 - 1492.

BACKGROUND: Horseweed is a weed commonly found in agronomic crops, waste areas and roadsides. Resistance to ALS-inhibiting herbicides in horseweed was first reported in 1993 in a population from Israel. Resistance to ALS-inhibiting herbicides in horseweed is now widespread, but, as of now, the resistance mechanism has not been reported. RESULTS: Two of three populations evaluated (P116 and P13) were found to be uniform for resistance (>98% of individuals survived 8.8 g AI ha^-1 of cloransulam), whereas a third population, P525, contained about 85% resistant individuals. Cross-resistance to cloransulam, chlorimuron, imazethapyr and bispyribac was observed in the P116 population. P525 and P13 were both sensitive to imazethapyr but resistant to chlorimuron, imazethapyr and bispyribac. Enzyme activity assays indicated that resistance in P13 was due to an altered target site. Southern blot analysis indicated that the ALS target site is encoded by a single copy gene. Overlapping ALS gene regions were amplified and sequenced from each population. Amino acid substitutions of Ser for Pro at position 197 (P197S) was detected from P13, Ala for Pro (P197A) was identified from P525 and substitution of Glu for Asp (D376E) at position 376 was found in P116. Molecular markers were developed to differentiate between wild-type and resistant codons at positions 197 and 376 of horseweed ALS. CONCLUSION: Resistance to ALS-inhibiting herbicides in horseweed is conferred by target-site mutations that have also been identified in other weed species. Identification of the mutations within horseweed ALS gene sequence enables molecular assays for rapid detection and resistance diagnosis..

Matzrafi, M., T. W. Lazar, M. Sibony, and B. Rubin. 2015. Conyza species: distribution and evolution of multiple target-site herbicide resistances. Planta 242 : 259 - 267.

Conyza canadensis (CC) and Conyza bonariensis (CB) are troublesome weeds around the world. Extensive use of herbicides has led to the evolution of numerous Conyza spp. herbicide-resistant populations. Seeds of 91 CC and CB populations were collected across Israel. They were mostly found (86 %) in roadsides and urban habitats, two disturbed habitats that had been dramatically impacted by human activities, thus we classify these species as anthropogenic. Although pyrithiobac-sodium was only used in cotton fields, 90 % of Conyza spp. populations were identified as pyrithiobac-sodium resistant, suggesting possible natural resistance to pyrithiobac-sodium. CC21 and CC17 C. canadensis populations were highly resistant to all tested ALS inhibitors due to a substitution in the ALS gene from Trp574 to Leu. They were also atrazine resistant due to a substitution in the psbA gene from Ser264 to Gly. The high level of imazapyr and pyrithiobac-sodium resistance observed in the CC10 population was due to an Ala205 to Val substitution. However, high resistance to sulfometuron methyl and pyrithiobac-sodium in population CC6 was due to a point mutation at Pro197 to Ser. All resistant plants of CC21 population showed both psbA (Ser264 to Gly) and ALS (Trp574 to Leu) substitutions, leading us to the conclusion that the attempt to overcome resistance to one mode of action by overuse of another will most likely lead to multiple herbicide resistance. Furthermore, we concluded that only individuals that carry both mutations could survive the shift between the two modes of action and overcome the fitness cost associated with the PSII resistance..

This case was entered by Patrick Tranel Email: tranel@illinois.edu

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