Breaking the biotrophic interfacial complex: How genome editing can lead to rice blast resistance.

Breaking the biotrophic interfacial complex: How genome editing can lead to rice blast resistance.
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打破生物营养界面复合体:基因组编辑如何导致稻瘟病抗性。

DOI:
10.1016/j.molp.2023.07.008
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发表时间:
2023
期刊:
影响因子:
27.5
通讯作者:
Were V
Were V
中科院分区:
生物学1区
文献类型:
--
作者:
Were V

文献摘要

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基因组编辑是一项变革性技术--通过精确地改变特定基因的编码或调控序列,现在可以改变各种生物体中的特定特征。因此,植物育种可以达到一个新的精确水平,许多国家正在迅速采取行动,通过新的立法来允许基因组编辑(Greenwood等人,2023年)。然而,到目前为止,基因组编辑很少被用于开发抗病作物。这是因为植物免疫通常依赖于单一的显性抗性基因,这些基因编码的免疫受体识别植物病原体部署的分泌效应器(Jones和Dangl,2006)。在这种背景下,到目前为止,转基因已被证明是一种更强大的技术,可以从不同的品种甚至不同物种中引入这些基因,以培育抗病作物物种(Greenwood等人,2023),特别是当多个抗病基因位点合在一起可以提供更持久的抗性时(Luo等人,2021)。基因组编辑可以以一种创新的方式用于复活以前有效的抗病基因(Contrera等人,2023),但在向作物引入新的抗病形式方面效果较差。然而,最近的一项研究表明,基因组编辑在识别和部署新的抗病来源方面具有巨大的潜力。李国天和帕梅拉·罗纳德的研究小组使用基因组编辑来表征一种与一种新形式的抗病相关的基因(沙等人,2023)。这项研究是在对病变模拟突变体的筛选中启动的。这些是突变体,在没有病原体的情况下会产生超敏反应样病变。这反映了当不相容的病原体被用来挑战耐药宿主时通常发生的情况。损伤模拟突变体已被用于深入了解与植物免疫相关的信号通路(Lorrain等人,2003年)。有趣的是,所鉴定的病斑模拟突变体与一个单基因有关,作者将该基因命名为对BLAST1(RBL1)的抗性,因为RBL1突变体被发现对稻瘟病菌具有抗性。稻瘟病是栽培水稻最具破坏性的疾病之一,在水稻种植的任何地方都是一个严重的问题(Eseola等人,2021年)。鉴于其对全球粮食安全的压倒性重要性,发现对稻瘟病的抗性将为确保全球粮食安全做出重要的潜在贡献。RBL1突变体对稻瘟病表现出显著的抗病能力。然而,像许多病斑模拟突变体一样,这也影响了寄主植物的适合性,导致产量减少20倍。这就是为什么如此多先前发现的病变模拟突变体已被证明不可能更广泛地部署(沙等人,2023)。然而,正是在这里,
Genome editing is a transformational technology—by precisely altering the coding or regulatory sequence of a specific gene, it is now possible to change specific traits within a wide variety of organisms. As a consequence, plant breeding can be taken to a new level of precision, and many countries are moving rapidly to adopt new legislation to permit genome editing (Greenwood et al., 2023). However, genome editing has so far seldom been used to develop disease-resistant crops. This is because plant immunity often depends on single dominant resistance genes, which encode immune receptors that recognize secreted effectors deployed by plant pathogens (Jones and Dangl, 2006). In this context, genetic modification has proven to be a much more powerful technology so far to introduce these genes from distinct varieties, or even different species, to develop disease resistant crop species (Greenwood et al., 2023), especially when multiple disease-resistance loci can be introduced together to provide more durable resistance (Luo et al., 2021). Genome editing can be used in an innovative way to resurrect previously effective resistance genes (Contreras et al., 2023), but it has been less effective at introducing new forms of disease resistance to crops.A recent study, however, has demonstrated the enormous potential of genome editing in identifying and deploying novel sources of disease resistance. Guotian Li’s and Pamela Ronald’s research groups have used genome editing to characterize a gene associated with a novel form of disease resistance (Sha et al., 2023). The study was initiated in a screen for lesion mimic mutants. These are mutants in which hypersensitive response-like lesions are generated in the absence of pathogens. This mirrors the situation that normally occurs when an incompatible pathogen is used to challenge a resistant host. Lesion mimic mutants have been used to provide insight into the signaling pathways associated with plant immunity (Lorrain et al., 2003). Interestingly, the lesion mimic mutant identified was associated with a single gene that the authors named RESISTANCE TO BLAST1 (RBL1) because RBL1 mutants were found to be resistant to the rice blast fungus Magnaporthe oryzae. Rice blast is one of the most devastating diseases of cultivated rice and a serious concern wherever rice is grown (Eseola et al., 2021). Given its overwhelming importance to global food security, finding resistance to blast—which also causes an emerging disease of wheat (Latorre et al., 2023)—would provide an important potential contribution toward ensuring global food security. RBL1 mutants showed a significant level of disease resistance to blast. However, like many lesion mimic mutants, this also affected the fitness of the host plant, leading to a 20-fold reduction in yield. This is the reason that so many lesion mimic mutants identified previously have proven impossible to deploy more widely (Sha et al., 2023). However, it is here that