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Weeds developing resistance to herbicides pose a significant threat to profitability, and undermine our ability to produce food and fuel crops and to meet many environmental objectives.
In general the more effective a herbicide is, the greater the risk of resistance.
The more herbicides that are used the lower is overall crop profitability, and the more likely it is that they will be found in water and that control will be so broad spectrum that too few desirable plant species survive.
Spring cropping, to counter severe grassweed resistance, may be good for biodiversity and reduce herbicide use, but it reduces production and leaves little profit.
So how can we move forward?
We must develop our understanding of resistance based on weed biology and herbicides impact.
We cant rely on new products becoming available, so we must strive to hold onto a wide range of useful ones.
Mixtures and sequences only delay resistance so we must use them effectively and efficiently alongside cost-effective cultural control.
We should also use all herbicides in a way that reduces risks to water quality.
Information is available to achieve both resistance and water quality objectives, but it must be readily accessible.
Which partner is best to use to delay resistance build-up to Atlantis?
Usually the advice is to use a residual like pendimethalin or trifluralin, but do they really contribute much when sprayed at 2-3 leaf stage. Would they be better applied earlier when they might actually take out blackgrass to reduce the pressure on Atlantis?
And what about Hawk? It’s pricing has come down significantly (see next week’s FW), and provided there isn’t fop-resistance in the population, you could argue it will control soem blackgrass when applied with Atlantis. But is it a good strategy to use two high-risk actives at the same time? Does it increase the chances of double target-site resistance (i.e. target site resistance to both fops and sulfonylureas (Atlantis). occurring?
Mike, in reply to both yours and Stephens questions, the best anti resistance strategy to any individual or family of products is not to use them.
Thats simply said of course and in reality we will use what works …the key point to remember is that while we use them we will select for resistance. The practical approach is to rotate the active type that we use for the target weeds. In BLW’s we can use hormones, these have earlier growth stage restrictions than SU’s but if an early germination occurs we can take the opportunity of using them to good effect and give the Ally/starane a rest. Likewise in blackgrass growers should use a range of actives and use rapid seed tests to check resistance status on THEIR OWN grassweed population. If IPU or Hawk was dropped because control taled off ask yourself when you last used them …they could offer a high level of control again now.
There is talk of pendimethalin effectiveness reducing …again, has it infact ever been used on your own grassweed population? if not you may get very high levels of control. With all products remember that EMR resistance developes as the plant matures so spray very early in the life of the plant, 1-3 leaves and look carefully at the application technique you use.
There is very limited evidence that EMR resistance actually develops as the weeds mature as the knowledge about the actual metabolic processes involved in resistant weeds is still poorly understood. Indeed we can pick up clear evidence of metabolic resistance to pendimethalin in germinating seeds. However, I would agree that in general that it is easier to kill small resistance plants than big ones, but there may be some exceptions to this. For example, small cold stressed blackgrass plants may not be well controlled by Atlantis whereas larger actively growing plants may be.
Another point is that mixtures and sequences should not be seen as a resistance prevention strategy, rather a delaying strategy. One only has to look at the history of ‘fop’ and ‘dim’ resistance which shows clearly that use of other herbicides in combination with them did not prevent resistance developing. Surveys indicate that resistance in black-grass to fops/dims occurs on most farms where herbicides have been sprayed regularly, and on virtually all of these fop/dims will have been used in mixture and sequence with many other herbicides in various crops (IPU, triallate, pendimethalin, trifluralin, propyzamide etc.). Their use did not stop resistance developing, so no one should be surprised if resistance to the ‘new kid on the block’ i.e. Atlantis, develops despite using mixtures and sequences of other herbicides. The problem is that whereas in the past there was a steady stream of new herbicides coming along to save the day, that does not seem to be the case now. There are new herbicides beining developed, but none appear to be band new modes of action, rather variations on a theme.
I hope I am not being too patronising here, but it strikes me that nearly all the comments on this forum are from people who are pretty well clued up and have a good grasp of the issues. The real problem is getting through to those who don’t!
I agree with all that you say …particularly your final point! I am not for a moment suggesting that we can prevent resistance building to an active and it maybe that readers of this forum understand a detailed explanation …as far as we know it, perfectly well but I often find that a simple presentation of some basic rules to delay resistance along as possible is more easily digested and acted upon.