Australian Herbicide Resistance Initiative (AHRI)

How do P450 enzymes cause resistance?

Researcher looking at samples

What is a P450? Is it a car from the 70’s that fits a 44 gallon drum in the boot? No, that would be a P76. A P450 is an enzyme that eats herbicides. In fact, there are literally hundreds of P450 enzymes and some of them can chew on some herbicides, resulting in enhanced herbicide metabolism (metabolic resistance).

We are now seeing an increased effort around the world to better understand metabolic resistance involving P450 enzymes. In 2005, Dr Paul Neve showed that ryegrass could quickly develop resistance after being sprayed with low doses of Hoegrass® (diclofop). Some recent AHRI research by Dr Qin Yu and others has now confirmed that this was due to enhanced metabolic resistance, likely involving P450 enzymes. Further AHRI research by Dr Ahmad-Hamdani confirmed the same result for a population of wild oats.

Wheat can tolerate herbicides such as diclofop by metabolic resistance. We now know that weeds such as ryegrass and wild oats also have the ability to evolve this mechanism of resistance.

What is metabolic resistance?

Herbicide resistance can be broadly grouped into two main mechanisms:

Target site resistance – where the herbicide can no longer bind to the target site due to a mutation in the plant.
Metabolic resistance – where the herbicide does not reach the target site because the plant metabolises (eats) the herbicide before it can get there. One type of metabolic resistance involves P450 enzymes.

Metabolic resistance p450s showing effects

Target site resistance is very well understood because it is relatively easy to research. Metabolic resistance research is more difficult and is therefore poorly understood.

Metabolic resistance research

At this stage there is no way of simply measuring P450 activity so AHRI researchers took the following steps to demonstrate that resistance is due to P450s:

Step 1: Confirm that the ryegrass populations studied do not have target site resistance to diclofop-methyl. They studied populations of ryegrass that were confirmed resistant and susceptible. The resistant populations were from Paul Neve’s low dose research. All populations were confirmed not containing target site resistance to diclofop.

Step 2: Confirm that foliar uptake and translocation were similar for all populations. The researchers used radio labelled [14C] diclofop-methyl to measure foliar uptake and translocation and confirmed that there was no difference between resistant (R) and susceptible (S) populations.

Step 3: This is the tricky bit. Measure the metabolism of [14C] diclofop-methyl by R and S populations. When diclofop-methyl enters the weed it is de-esterfied into diclofop acid. This acid is the compound that kills the plant. In this case, the AHRI researchers found that a few days after treatment there was less diclofop acid present in the R plants than the S plants. The resistant plants had broken down the diclofop acid into harmless metabolites faster than the susceptible plants. This is likely due to the resistant plants having higher levels of the P450 enzymes that degrade diclofop acid.

As there is currently no simple way of measuring the exact level of a particular P450 enzyme, we can only say that it is ‘likely’ to be the cause of resistance. It is thought that several different P450s may be involved in causing this resistance. Future research will provide more precise answers to these questions.

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