Integrated multi-omic analysis of host-microbiota interactions in acute oak decline.
Integrated multi-omic analysis of host-microbiota interactions in acute oak decline.
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DOI：
10.1186/s40168-018-0408-5
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发表时间：
2018-01-30
期刊：
影响因子：
15.5
通讯作者：
McDonald JE
中科院分区：
文献类型：
--
作者：
Broberg M;Doonan J;Mundt F;Denman S;McDonald JE
英国本土的橡树物种目前正受到急性橡树衰退（AOD）的威胁，这是一种衰退疾病，其主要症状是树干出血覆盖在树皮内部的坏死病变和树皮蛀皮甲虫（Agrilus biguttatus）的幼虫通道上。众所周知，植物寄主与其微生物群（即全息生物）之间的复杂相互作用显著影响植物的健康状况。在AOD中，坏死病变是由微生物群转移到主要由goodwinii Brenneria， quercinecans Gibbsiella， victoriarahnella和潜在的其他细菌组成的致病群引起的。然而，微生物群引起组织坏死的具体机制过程和宿主反应尚未确定，这是理解和管理这种衰退的障碍。我们分析了AOD症状树和非症状树树皮内部组织的元基因组、元转录组和元蛋白质组，以表征微生物与宿主的相互作用。在AOD病变中发现了活性细菌毒力因子，如植物细胞壁降解酶、活性氧防御和鞭毛，以及宿主防御反应，包括活性氧、细胞壁修饰和防御调节因子。B. goodwinii在病变菌群中占主导地位，其毒力因子如植物病原菌效应物avrE的表达显著。槲皮菌和维多利亚菌的微生物活性比例较小。此外，我们首次描述了两种以前未被描述的革兰氏阳性细菌的潜在作用，这些细菌是由宏基因组分析预测的，并被鉴定为在AOD病变的元转录组和元蛋白质组中活跃，暗示它们在病变形成中起作用。这项多组学研究为AOD中微生物-宿主相互作用提供了新的功能见解，AOD是一种复杂的树木衰退疾病，多微生物-宿主相互作用导致树干病变形成。我们首次描述了holobiont在橡树健康和疾病中的作用，特别是goodwinii， G. quercinecans， Rahnella victoria和其他细菌的相对损害活性。因此，本文提出的研究为病变微生物组成员使用的一些机制提供了证据，并为未来的多组学研究提供了模板，以研究全生物特性、植物多微生物疾病和树木的病原体防御。本文的在线版本（10.1186/s40168-018-0408-5）包含补充材料，可供授权用户使用。
Britain’s native oak species are currently under threat from acute oak decline (AOD), a decline-disease where stem bleeds overlying necrotic lesions in the inner bark and larval galleries of the bark-boring beetle, Agrilus biguttatus, represent the primary symptoms. It is known that complex interactions between the plant host and its microbiome, i.e. the holobiont, significantly influence the health status of the plant. In AOD, necrotic lesions are caused by a microbiome shift to a pathobiome consisting predominantly of Brenneria goodwinii, Gibbsiella quercinecans, Rahnella victoriana and potentially other bacteria. However, the specific mechanistic processes of the microbiota causing tissue necrosis, and the host response, have not been established and represent a barrier to understanding and managing this decline. We profiled the metagenome, metatranscriptome and metaproteome of inner bark tissue from AOD symptomatic and non-symptomatic trees to characterise microbiota-host interactions. Active bacterial virulence factors such as plant cell wall-degrading enzymes, reactive oxygen species defence and flagella in AOD lesions, along with host defence responses including reactive oxygen species, cell wall modification and defence regulators were identified. B. goodwinii dominated the lesion microbiome, with significant expression of virulence factors such as the phytopathogen effector avrE. A smaller proportion of microbiome activity was attributed to G. quercinecans and R. victoriana. In addition, we describe for the first time the potential role of two previously uncharacterised Gram-positive bacteria predicted from metagenomic binning and identified as active in the AOD lesion metatranscriptome and metaproteome, implicating them in lesion formation. This multi-omic study provides novel functional insights into microbiota-host interactions in AOD, a complex arboreal decline disease where polymicrobial-host interactions result in lesion formation on tree stems. We present the first descriptions of holobiont function in oak health and disease, specifically, the relative lesion activity of B. goodwinii, G. quercinecans, Rahnella victoriana and other bacteria. Thus, the research presented here provides evidence of some of the mechanisms used by members of the lesion microbiome and a template for future multi-omic research into holobiont characterisation, plant polymicrobial diseases and pathogen defence in trees. The online version of this article (10.1186/s40168-018-0408-5) contains supplementary material, which is available to authorized users.
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影响因子：
2.9
作者：
Brown, Nathan;Jeger, Mike;Denman, Sandra
通讯作者：
Denman, Sandra
影响因子：
3.4
作者：
Denman, Sandra;Plummer, Sarah;McDonald, James E.
通讯作者：
McDonald, James E.
DOI：
10.1038/nrmicro3451
发表时间：
2015-06
期刊：
Nature reviews. Microbiology
影响因子：
--
作者：
Franzosa EA;Hsu T;Sirota-Madi A;Shafquat A;Abu-Ali G;Morgan XC;Huttenhower C
通讯作者：
Huttenhower C
影响因子：
30.3
作者：
Bulgarelli D;Garrido-Oter R;Münch PC;Weiman A;Dröge J;Pan Y;McHardy AC;Schulze-Lefert P
通讯作者：
Schulze-Lefert P
影响因子：
14.8
作者：
通讯作者：
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