Microbial pathogens trigger host DNA double-strand breaks whose abundance is reduced by plant defense responses.
Microbial pathogens trigger host DNA double-strand breaks whose abundance is reduced by plant defense responses.
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DOI：
10.1371/journal.ppat.1004030
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发表时间：
2014-04
期刊：
影响因子：
6.7
通讯作者：
Bent AF
中科院分区：
文献类型：
--
作者：
Song J;Bent AF
免疫反应和DNA损伤修复是两个基本过程，已被广泛表征，但它们之间的联系在很大程度上仍然未知。我们报告了多种细菌、真菌和卵菌植物病原体物种诱导宿主植物DNA双链断裂（DSB）。通过组蛋白γ-H2 AX丰度或DNA彗星试验检测到的DNA损伤发生在致病性假单胞菌引起的疾病相关坏死前数小时。番茄在施用后的类似阶段，诱导坏死的百草枯未引起可检测到的DSB。非致病性E.大肠杆菌和荧光假单胞菌也不诱导DSB。活性氧（reactive oxygen species，ROS）的升高是植物免疫应答过程中常见的现象，ROS是已知的DNA损伤因子，在动物实验中，感染诱导的宿主ROS爆发是导致宿主DNA损伤的原因之一。然而，我们发现，在拟南芥中DSB的形成响应于P. dichlingae感染仍然发生在感染相关的氧化猝发的AtrbohD和AtrbohF介导的情况下。植物MAMP受体刺激或应用防御激活水杨酸或茉莉酸未能诱导可检测水平的DSB在引入的病原体的情况下，进一步表明病原体活动超出宿主防御激活引起感染诱导的DNA损伤。水杨酸和NPR 1介导的防御以及某些R基因介导的防御降低了感染诱导的DSB的丰度。拟南芥atr/atm双突变体中仍然存在病原菌诱导的γ-H2 AX的形成，表明病原菌诱导的H2 AX磷酸化的替代介质的存在。综上所述，病原微生物可以诱导植物DNA损伤。植物防御机制有助于抑制而不是促进这种损害，从而有助于维持体细胞组织中基因组的完整性。多细胞生物持续暴露于微生物，并已发展出复杂的防御机制来抵抗微生物病原体的攻击。生物体也会遇到许多类型的DNA损伤，并进化出多种机制来维持其基因组的完整性。尽管这两种基本反应已被广泛描述，但它们之间的关系在很大程度上仍不清楚。我们的研究表明，具有不同生活方式的微生物植物病原体，包括细菌，卵菌和真菌病原体，诱导双链断裂（DSB）在受感染的宿主植物细胞的基因组。DSB诱导是植物与病原菌互作过程中的一个共同特征。DSB是最有害的DNA损伤形式，可导致染色体畸变和基因突变。植物对病原体感染的反应是激活免疫反应，并有助于抑制病原体诱导的DSB，从而保持更好的基因组完整性和稳定性。这些发现确定了植物免疫和DNA损伤修复反应相互关联的重要方式。对上述现象的认识可能会促进未来疾病管理方法的发展，提高作物在生物胁迫下的生产力。
Immune responses and DNA damage repair are two fundamental processes that have been characterized extensively, but the links between them remain largely unknown. We report that multiple bacterial, fungal and oomycete plant pathogen species induce double-strand breaks (DSBs) in host plant DNA. DNA damage detected by histone γ-H2AX abundance or DNA comet assays arose hours before the disease-associated necrosis caused by virulent Pseudomonas syringae pv. tomato. Necrosis-inducing paraquat did not cause detectable DSBs at similar stages after application. Non-pathogenic E. coli and Pseudomonas fluorescens bacteria also did not induce DSBs. Elevation of reactive oxygen species (ROS) is common during plant immune responses, ROS are known DNA damaging agents, and the infection-induced host ROS burst has been implicated as a cause of host DNA damage in animal studies. However, we found that DSB formation in Arabidopsis in response to P. syringae infection still occurs in the absence of the infection-associated oxidative burst mediated by AtrbohD and AtrbohF. Plant MAMP receptor stimulation or application of defense-activating salicylic acid or jasmonic acid failed to induce a detectable level of DSBs in the absence of introduced pathogens, further suggesting that pathogen activities beyond host defense activation cause infection-induced DNA damage. The abundance of infection-induced DSBs was reduced by salicylic acid and NPR1-mediated defenses, and by certain R gene-mediated defenses. Infection-induced formation of γ-H2AX still occurred in Arabidopsis atr/atm double mutants, suggesting the presence of an alternative mediator of pathogen-induced H2AX phosphorylation. In summary, pathogenic microorganisms can induce plant DNA damage. Plant defense mechanisms help to suppress rather than promote this damage, thereby contributing to the maintenance of genome integrity in somatic tissues. Multicellular organisms are continuously exposed to microbes and have developed sophisticated defense mechanisms to counter attack by microbial pathogens. Organisms also encounter many types of DNA damage and have evolved multiple mechanisms to maintain their genomic integrity. Even though these two fundamental responses have been characterized extensively, the relationship between them remains largely unclear. Our study demonstrates that microbial plant pathogens with diverse life styles, including bacteria, oomycete and fungal pathogens, induce double-strand breaks (DSBs) in the genomes of infected host plant cells. DSB induction is apparently a common feature during plant-pathogen interactions. DSBs are the most deleterious form of DNA damage and can lead to chromosomal aberrations and gene mutations. In response to pathogen infection, plant immune responses are activated and contribute to suppressing pathogen-induced DSBs, thereby maintaining better genome integrity and stability. The findings identify important ways that the plant immune and DNA damage repair responses are interconnected. Awareness of the above phenomena may foster future development of disease management approaches that improve crop productivity under biotic stress.
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影响因子：
--
作者：
Chakraborty SP;Kar Mahapatra S;Sahu SK;Das S;Tripathy S;Dash S;Pramanik P;Roy S
通讯作者：
Roy S
影响因子：
11.3
作者：
Ambur OH;Davidsen T;Frye SA;Balasingham SV;Lagesen K;Rognes T;Tønjum T
通讯作者：
Tønjum T
DOI：
10.1094/mpmi-21-10-1285
发表时间：
2008-10
期刊：
Molecular plant-microbe interactions : MPMI
影响因子：
--
作者：
Genger RK;Jurkowski GI;McDowell JM;Lu H;Jung HW;Greenberg JT;Bent AF
通讯作者：
Bent AF
影响因子：
11.6
作者：
Amiard, Simon;Depeiges, Annie;Gallego, Maria Eugenia
通讯作者：
Gallego, Maria Eugenia
影响因子：
11.6
作者：
CAO, H;BOWLING, SA;DONG, XN
通讯作者：
DONG, XN