Quantitative interactions: the disease outcome of Botrytis cinerea across the plant kingdom.
Quantitative interactions: the disease outcome of Botrytis cinerea across the plant kingdom.
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DOI：
10.1093/g3journal/jkab175
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发表时间：
2021-08-07
期刊：
影响因子：
--
通讯作者：
Kliebenstein DJ
中科院分区：
文献类型：
--
作者：
Caseys C;Shi G;Soltis N;Gwinner R;Corwin J;Atwell S;Kliebenstein DJ
灰霉病菌是一种真菌病原体，可在广泛分布于植物界的1000多个已知寄主上引起坏死性疾病。灰霉菌如何与如此广泛的寄主多样性相互作用在很大程度上尚不清楚。为了解决这个问题，我们生成了代表8种寄主植物的90种基因型的98株灰霉菌的感染性矩阵。这一实验感染性矩阵显示，疾病结果在很大程度上是由寄主抗性或病原菌毒力的变化来解释的。然而，宿主和病原体之间的特定相互作用占疾病结果的16%。此外，疾病结果在一个物种的基因类型之间聚集，但与宿主之间的亲缘关系无关。在分析灰霉菌的寄主专一性和毒力时，通用型菌株占主导地位。在这种真菌嗜死菌中，特化可能是由于大多数宿主的毒力下降而不是特定宿主的毒力增加而发生的。为了揭示灰霉病菌寄主特异性和致病力的遗传结构，进行了全基因组关联研究，发现了多达1492个感兴趣的基因。这些特征的遗传结构广泛存在于灰霉病菌基因组中。疾病结果的复杂性可能是由数百个功能不同的基因解释的，这些基因被认为参与了调节感染以适应不同宿主的过程。
Botrytis cinerea is a fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. How B. cinerea interacts with such extensive host diversity remains largely unknown. To address this question, we generated an infectivity matrix of 98 strains of B. cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix revealed that the disease outcome is largely explained by variations in either the host resistance or pathogen virulence. However, the specific interactions between host and pathogen account for 16% of the disease outcome. Furthermore, the disease outcomes cluster among genotypes of a species but are independent of the relatedness between hosts. When analyzing the host specificity and virulence of B. cinerea, generalist strains are predominant. In this fungal necrotroph, specialization may happen by a loss in virulence on most hosts rather than an increase of virulence on a specific host. To uncover the genetic architecture of Botrytis host specificity and virulence, a genome-wide association study (GWAS) was performed and revealed up to 1492 genes of interest. The genetic architecture of these traits is widespread across the B. cinerea genome. The complexity of the disease outcome might be explained by hundreds of functionally diverse genes putatively involved in adjusting the infection to diverse hosts.
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