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急性栎树衰退病理生物群中细菌的基因组分析。

Genomic analysis of bacteria in the Acute Oak Decline pathobiome.

机构信息

1​School of Biological Sciences, Bangor University, Bangor, UK.

2​Forest Research, Centre for Forestry and Climate Change, Farnham, UK.

出版信息

Microb Genom. 2019 Jan;5(1). doi: 10.1099/mgen.0.000240.

DOI:10.1099/mgen.0.000240
PMID:30625111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6412055/
Abstract

The UK's native oak is under serious threat from Acute Oak Decline (AOD). Stem tissue necrosis is a primary symptom of AOD and several bacteria are associated with necrotic lesions. Two members of the lesion pathobiome, Brenneria goodwinii and Gibbsiella quercinecans, have been identified as causative agents of tissue necrosis. However, additional bacteria including Lonsdalea britannica and Rahnella species have been detected in the lesion microbiome, but their role in tissue degradation is unclear. Consequently, information on potential genome-encoded mechanisms for tissue necrosis is critical to understand the role and mechanisms used by bacterial members of the lesion pathobiome in the aetiology of AOD. Here, the whole genomes of bacteria isolated from AOD-affected trees were sequenced, annotated and compared against canonical bacterial phytopathogens and non-pathogenic symbionts. Using orthologous gene inference methods, shared virulence genes that retain the same function were identified. Furthermore, functional annotation of phytopathogenic virulence genes demonstrated that all studied members of the AOD lesion microbiota possessed genes associated with phytopathogens. However, the genome of B. goodwinii was the most characteristic of a necrogenic phytopathogen, corroborating previous pathological and metatranscriptomic studies that implicate it as the key causal agent of AOD lesions. Furthermore, we investigated the genome sequences of other AOD lesion microbiota to understand the potential ability of microbes to cause disease or contribute to pathogenic potential of organisms isolated from this complex pathobiome. The role of these members remains uncertain but some such as G. quercinecans may contribute to tissue necrosis through the release of necrotizing enzymes and may help more dangerous pathogens activate and realize their pathogenic potential or they may contribute as secondary/opportunistic pathogens with the potential to act as accessory species for B. goodwinii. We demonstrate that in combination with ecological data, whole genome sequencing provides key insights into the pathogenic potential of bacterial species whether they be phytopathogens, part-contributors or stimulators of the pathobiome.

摘要

英国本土栎树受到急性栎树衰退(AOD)的严重威胁。茎组织坏死是 AOD 的主要症状,几种细菌与坏死病变有关。病变病理生物群的两个成员 Brenneria goodwinii 和 Gibbsiella quercinecans 已被确定为组织坏死的病原体。然而,在病变微生物组中还检测到了其他细菌,包括 Lonsdalea britannica 和 Rahnella 种,但它们在组织降解中的作用尚不清楚。因此,了解潜在的基因组编码组织坏死机制对于理解病变病理生物群中细菌成员在 AOD 病因学中的作用和机制至关重要。在这里,从 AOD 感染的树木中分离出的细菌的全基因组被测序、注释,并与典型的植物病原菌和非致病性共生体进行了比较。使用同源基因推断方法,鉴定出保留相同功能的共享毒力基因。此外,对植物病原菌毒力基因的功能注释表明,AOD 病变微生物群的所有研究成员都具有与植物病原菌相关的基因。然而,B. goodwinii 的基因组最具坏死植物病原菌的特征,这与先前的病理学和宏转录组学研究结果一致,这些研究结果表明它是 AOD 病变的关键病原体。此外,我们还研究了其他 AOD 病变微生物组的基因组序列,以了解微生物引起疾病的潜在能力或对从这个复杂病理生物群中分离出的生物体的致病潜力的贡献。这些成员的作用仍然不确定,但有些成员,如 G. quercinecans,可能通过释放坏死酶导致组织坏死,并有助于更危险的病原体激活并实现其致病潜力,或者它们可能作为次要/机会性病原体发挥作用,有可能作为 B. goodwinii 的辅助物种。我们证明,结合生态数据,全基因组测序为细菌物种的致病潜力提供了关键的见解,无论它们是植物病原菌、部分贡献者还是病理生物群的刺激物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/cccf1bf7f0cf/mgen-5-240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/1482314225b7/mgen-5-240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/6998a2de0c1d/mgen-5-240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/4a268c94453a/mgen-5-240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/cccf1bf7f0cf/mgen-5-240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/1482314225b7/mgen-5-240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/6998a2de0c1d/mgen-5-240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/4a268c94453a/mgen-5-240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e1/6412055/cccf1bf7f0cf/mgen-5-240-g004.jpg

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