Herbicide resistance Eastern Black Nightshades
are a problem, but solutions are in sight.

Since 1999, several populations of eastern black nightshade from different location in Ontario have been reported as not being controlled by group 2 herbicides. Subsequent diagnostic tests at the University of Guelph confirmed resistance to imazethapyr (Pursuit) at 0.168 L/ac. Since discovery of the initial resistant population in Elgin County, resistant eastern black nightshade populations have also been confirmed in Middlesex, Huron, and Kent Counties.

To understand how resistant these weed populations were, dose response curves was developed by applying common post-emergence Group 2 herbicides at increasing rates to the initial resistant population from Elgin County. The results of those dose response experiments identified 750-fold resistance to imazethapyr (Pursuit), and lower resistance level to the other Group 2 herbicides in that resistant population.

Pre-emergence applications of imazethapyr (pursuit) did not provide control of the resistant population while they totally controlled the susceptible population (Table 1).

Table 1. Response of resistant and susceptible populations to a pre-emergence application of imazethapyr (Pursuit). Control was expressed on a scale from 0 to 100, with 0 meaning no effect and 100 meaning complete reduction of emergence.

This shows that resistance is likely due to internal changes in the resistant plants and does not involve differences in leaf uptake or movement of the herbicides. Therefore, we further looked at the molecular basis of resistance in those populations to better understand the cause and possible management options for this resistance problem.

Molecular basis for resistance

In other weeds, resistance to group 2 herbicides is most often conferred by a single change in the gene that codes for the target enzyme of the herbicide. All Group 2 herbicides kill susceptible plants by stopping the activity of the essential enzyme acetolactate synthase (ALS). This action prevents the formation of some amino acids and leads to protein starvation and death. Resistant plants have a mutation in the ALS gene that codes for a single amino acid change in the ALS enzyme. This change prevents the herbicide from binding to the enzyme and the plant can survive. One particularity of the ALS gene is that many different single mutations are possible, each conferring different spectrum of resistance. We therefore attempted to isolate and sequence the ALS gene from all the resistant populations in order to compare them to the susceptible populations.

The ALS sequence of all six resistant populations differed from that of the susceptible by only one nucleotide. All the resistant populations had the same mutation that codes for a valine substituting for an alanine at position 205 of the ALS gene. This shows that all resistant populations we have characterized will have the same response to the Group 2 herbicides.

Group 2 resistant Eastern black nightshade populations exist not only in Ontario but have also been found in Wisconsin, North Dakota, Illinois and Indiana. It is noteworthy though that our populations are likely to be different from those in the USA. Because the ALS mutation in Ontario populations was different from that found in the Illinois and Indiana populations, which was at position 122 of the gene. Furthermore, the Wisconsin and Illinois populations have resistance only to one class, while the Ontario populations have resistance to at least three classes of group 2 herbicides. This suggests that they are possibly the result of local selection and not from seed movement from the USA. Therefore, in order to reduce the selection pressure responsible for selecting Group 2 resistant populations of eastern black nightshade, herbicide rotation would be essential for growers.

Implications for management

We have conducted greenhouse tests on the efficacy of non-group 2 herbicides in order to determine whether they remain efficient at controlling these resistant nightshade populations. Pre-emergence application of metolachlor (Dual) and dimethenamid (Frontier) provided high control of the resistant and susceptible populations (Table 2). This shows that the mechanism conferring resistance to Group 2 herbicides is likely to be specific to that group and will not change the response to other herbicide groups.

Table 2. Response of resistant and susceptible Eastern-black nightshade to pre-emergence application chloroacetamide herbicides. Control was expressed on a scale from 0 to 100, with 0 meaning no effect and 100 meaning complete reduction of emergence.

Future directions

Under herbicide selection pressure, resistant populations could experience rapid population growth as they are being released from the competition of herbicide susceptible weeds.
This would be similar to an introduced plant invading a new habitat where it suffers from little competition and has no natural enemies. From an evolutionary point of view however, the resistant populations should have some fitness penalty compared to susceptible counterparts. In the absence of herbicides, this penalty would result in less offspring being produced.

While fitness penalties had to exist in resistant populations, their true extent has been the subject of some debate. This is because small differences between resistant and susceptible plants might be difficult to detect, although they remain biologically significant. Resistant plants should logically be less fit, otherwise they would be much more present in unsprayed populations than they actually are.

Understanding the nature, causes and extent of fitness differences between the resistant and susceptible populations is one of our current research goals. Knowing when fitness penalties are expressed (i.e. at the seed, seedling or mature stage) could help us devising management strategies that would exploit the weaknesses in the weeds life cycle.

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