New Technologies to Combat Herbicide Resistance
New Technologies to Combat Herbicide Resistance
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DOI：
10.1564/v30_apr_09
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发表时间：
2020-04
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通讯作者：
R. Edwards
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文献类型：
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作者：
R. Edwards
利用现代化学和生物技术来对抗耐药性？我认为这个问题的答案很明显是否定的；如果我们选择开发它们，解决方案就在拐角处。当细菌或动物对数百万美元的药物产生抗药性时，我们不会放弃治疗。相反，科学家建立了抗性机制，并开发了抑制它们的化学或生物治疗方法。例如，对青霉素和相关化学物质的耐药性促使了Augmentin的开发，Augmentin是一种抑制致病菌内酰胺酶的药物，可使这类抗生素失活（Gatadi et al., 2019）。同样，在人类癌症治疗中，肿瘤中多重耐药的发展导致了靶向和灭活耐受性机制的药物的开发（Ruzza等，2009）。在这两种情况下，这些新干预措施的关键是利用最好的科学来了解耐药性的分子基础，然后化学家可以针对这些基础进行选择性抑制。杂草科学家现在第一次对除草剂抗性获得了类似的见解，为针对这种破坏性性状开辟了新的可能性。为了破坏除草剂的抗性，我们首先需要了解它。杂草通过两种主要机制进化出对除草剂的耐受性（Yu & Powles 2014），称为靶点抗性（TSR）和非靶点抗性（NTSR）。在TSR中，除草剂靶向蛋白编码基因的突变导致酶或结构多肽的合成，这些酶或结构多肽对化学抑制的敏感性降低。如果该蛋白在植物中仍然具有功能，TSR提供了一种快速而强大的进化途径来抵抗特定类型的真菌
to use modern chemical and biological technology to counter resistance? I would argue the answer to that question is most patently no; solutions are around the corner if we choose to develop them. When bacteria or animals become resistant to multimillion dollar drugs, we do not abandon the therapy. Rather scientists establish the resistance mechanisms and develop chemical or biological treatments that suppress them. For example, the development of resistance to penicillin and related chemistries prompted the development of Augmentin, a drug that inhibited the lactamase enzyme in pathogenic bacteria that inactivated this class of antibiotics (reviewed by Gatadi et al., 2019). Similarly, in human cancer therapy, the development in multiple drug resistance in tumours has led to the development of drugs that target and inactivate the tolerance mechanism (Ruzza et al., 2009). In both cases, the key to these new interventions was to use the very best science to understand the molecular basis of drug resistance, which chemists could then target for selective inhibition. For the first time weed scientists are now gaining similar insights into herbicide resistance, opening up new possibilities to target this damaging trait. To disrupt herbicide resistance we first need to understand it. Weeds evolve tolerance to herbicides through two overarching mechanisms (Yu & Powles 2014), termed target site resistance (TSR) and non-target site resistance (NTSR). In TSR, mutations in the genes encoding proteins targeted by herbicides result in the synthesis of enzymes, or structural polypeptides that show reduced sensitivity to chemical inhibition. Providing the protein is still functional in the plant, TSR provides a rapid and powerful evolutionary route to resistance to the specific class of