Illustration of water chickweed entangled in DNA, symbolizing herbicide resistance.

Weed Resistance Breakthrough: New Strategies to Combat Tribenuron-Methyl

"Scientists identify key resistance mechanisms in Myosoton aquaticum, paving the way for innovative herbicide management"


In the ongoing battle between agriculture and weeds, herbicide resistance continues to pose a significant challenge. One particularly troublesome weed, Myosoton aquaticum (water chickweed), has developed resistance to multiple herbicides, including tribenuron-methyl, threatening crop yields and increasing the need for more intensive weed management strategies.

A recent study published in Pesticide Biochemistry and Physiology sheds light on the mechanisms behind this resistance, offering valuable insights for developing more effective weed control methods. The research focuses on a population of M. aquaticum (AH03) found to be highly resistant to tribenuron-methyl and other ALS-inhibiting herbicides.

This article will explore the key findings of the study, focusing on the target-site mutations and non-target-site mechanisms that contribute to tribenuron-methyl resistance in M. aquaticum. Understanding these mechanisms is crucial for devising strategies to overcome resistance and maintain the effectiveness of herbicides in agricultural systems.

Decoding the Resistance: How Water Chickweed Evades Herbicides

Illustration of water chickweed entangled in DNA, symbolizing herbicide resistance.

The research pinpoints two primary mechanisms driving tribenuron-methyl resistance in the AH03 population of M. aquaticum: target-site resistance (TSR) and non-target-site resistance (NTSR). TSR involves alterations in the herbicide's target enzyme, acetolactate synthase (ALS), preventing the herbicide from binding effectively. NTSR, on the other hand, encompasses various metabolic processes that reduce the amount of herbicide reaching the target site or detoxify the herbicide before it can cause damage.

Specifically, the study identified a Pro197Ala mutation in the ALS gene of the resistant M. aquaticum plants. This mutation, where the amino acid proline at position 197 is replaced by alanine, significantly reduces the sensitivity of the ALS enzyme to tribenuron-methyl. In vitro ALS assays confirmed that the ALS enzyme from the resistant plants was much less inhibited by tribenuron-methyl compared to the enzyme from susceptible plants.

  • P450-Mediated Metabolism: Pretreatment with malathion, an inhibitor of cytochrome P450 enzymes, partially reversed tribenuron-methyl resistance in the AH03 population, suggesting that enhanced metabolism by P450s plays a role in NTSR.
  • Glutathione-S-Transferases (GSTs): While GST activity could be induced by tribenuron-methyl in both resistant and susceptible populations, the resistant population had lower basal and induced GST activity, suggesting that GSTs may not be a primary factor in NTSR in this case.
  • Multiple Resistance: The AH03 population exhibited cross-resistance to other ALS-inhibiting herbicides, including pyrithiobac-sodium, florasulam, pyroxsulam, and flucarbazone-Na, as well as reduced sensitivity to diflufenican, indicating a complex resistance profile.
To facilitate rapid identification of resistant plants, the researchers developed a cleaved amplified polymorphic sequence (CAPS) marker specific to the Pro197Ala mutation. This marker allows for quick and accurate screening of M. aquaticum populations to determine the presence and frequency of the resistance-conferring mutation.

Toward Sustainable Weed Control: What's Next?

This research highlights the complex mechanisms underlying herbicide resistance in M. aquaticum, emphasizing the importance of understanding both target-site and non-target-site factors. The identification of the Pro197Ala mutation and the development of a CAPS marker provide valuable tools for monitoring resistance and guiding weed management decisions.

To combat herbicide resistance effectively, integrated weed management (IWM) strategies are crucial. These strategies combine multiple approaches, such as crop rotation, tillage, competitive cultivars, and herbicides with different modes of action, to reduce selection pressure and prevent the evolution of resistance.

Further research is needed to fully elucidate the role of P450 enzymes and other potential NTSR mechanisms in M. aquaticum. By gaining a deeper understanding of these processes, scientists can develop novel strategies to overcome resistance and ensure the long-term effectiveness of herbicides in agricultural systems, promoting sustainable crop production and minimizing environmental impact.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1016/j.pestbp.2018.12.004, Alternate LINK

Title: Target-Site And Non-Target-Site-Based Resistance To Tribenuron-Methyl In Multiply-Resistant Myosoton Aquaticum L.

Subject: Health, Toxicology and Mutagenesis

Journal: Pesticide Biochemistry and Physiology

Publisher: Elsevier BV

Authors: Shuang Bai, Fengwen Zhang, Zuren Li, Hengzhi Wang, Qian Wang, Jinxin Wang, Weitang Liu, Lianyang Bai

Published: 2019-03-01

Everything You Need To Know

1

What are the main ways water chickweed (*Myosoton aquaticum*) becomes resistant to tribenuron-methyl?

The AH03 population of *M. aquaticum* (water chickweed) has developed resistance through two primary mechanisms: target-site resistance (TSR) and non-target-site resistance (NTSR). Target-site resistance involves alterations in the acetolactate synthase (ALS) enzyme, while non-target-site resistance includes metabolic processes like those involving P450 enzymes.

2

What specific genetic change in water chickweed (*Myosoton aquaticum*) makes it resistant to tribenuron-methyl, and how was this confirmed?

The study identified a Pro197Ala mutation in the ALS gene of the resistant *M. aquaticum*. This mutation means the amino acid proline at position 197 is replaced by alanine, significantly reducing the sensitivity of the ALS enzyme to tribenuron-methyl. This was confirmed through *in vitro* ALS assays.

3

How do cytochrome P450 enzymes contribute to tribenuron-methyl resistance in water chickweed (*Myosoton aquaticum*)?

Cytochrome P450 enzymes are involved in non-target-site resistance (NTSR). Pretreatment with malathion, which inhibits cytochrome P450 enzymes, partially reversed resistance to tribenuron-methyl in the AH03 population. This suggests that enhanced metabolism by P450s plays a role in the detoxification or breakdown of the herbicide before it can reach its target.

4

How can scientists quickly identify water chickweed (*Myosoton aquaticum*) plants that are resistant to tribenuron-methyl?

A cleaved amplified polymorphic sequence (CAPS) marker specific to the Pro197Ala mutation was developed. This marker allows for quick and accurate screening of *M. aquaticum* populations to determine the presence and frequency of the resistance-conferring mutation. This is important for monitoring resistance spread and guiding weed management strategies.

5

Does the AH03 population of water chickweed (*Myosoton aquaticum*) show resistance to other herbicides besides tribenuron-methyl?

The AH03 population of *M. aquaticum* exhibits cross-resistance to other ALS-inhibiting herbicides, including pyrithiobac-sodium, florasulam, pyroxsulam, and flucarbazone-Na. It also shows reduced sensitivity to diflufenican. This complex resistance profile highlights the challenge in controlling this weed and suggests that relying on a single class of herbicides will not be effective.

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