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转录组分析揭示了苹果腐烂病菌对生防放线菌杨凌链霉菌 Hhs.015 的响应机制。

Transcriptome analysis of Valsa mali reveals its response mechanism to the biocontrol actinomycete Saccharothrix yanglingensis Hhs.015.

机构信息

State Key Laboratory of Crop Stress Biology for Arid Areas, Northwest A&F University, Yangling, Shaanxi, China.

College of Life Science, Northwest A&F University, Yangling, Shaanxi, China.

出版信息

BMC Microbiol. 2018 Aug 22;18(1):90. doi: 10.1186/s12866-018-1225-5.

DOI:10.1186/s12866-018-1225-5
PMID:30134836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6106759/
Abstract

BACKGROUND

Apple canker is a devastating branch disease caused by Valsa mali (Vm). The endophytic actinomycete Saccharothrix yanglingensis Hhs.015 (Sy Hhs.015) can effectively inhibit the growth of Vm. To reveal the mechanism, by which Vm respond to Sy Hhs.015, the transcriptome of Vm was analyzed using RNA-seq technology.

RESULTS

Compared with normal growing Vm in the control group, 1476 genes were significantly differentially expressed in the Sy Hhs.015's treatment group, of which 851 genes were up-regulated and 625 genes were down-regulated. Combined gene function and pathway analysis of differentially expressed genes (DEGs) revealed that Sy Hhs.015 affected the carbohydrate metabolic pathway, which is utilized by Vm for energy production. Approximately 82% of the glycoside hydrolase genes were down-regulated, including three pectinase genes (PGs), which are key pathogenic factors. The cell wall structure of Vm was disrupted by Sy Hhs.015 and cell wall-related genes were found to be down-regulated. Of the peroxisome associated genes, those encoding catalase (CAT) and superoxide dismutase (SOD) which scavenge reactive oxygen species (ROS), as well as those encoding AMACR and ACAA1 which are related to the β-oxidation of fatty acids, were down-regulated. MS and ICL, key genes in glyoxylate cycle, were also down-regulated. In response to the stress of Sy Hhs.015 exposure, Vm increased amino acid metabolism to synthesize the required nitrogenous compounds, while alpha-keto acids, which involved in the TCA cycle, could be used to produce energy by deamination or transamination. Retinol dehydrogenase, associated with cell wall dextran synthesis, and sterol 24-C-methyltransferase, related to cell membrane ergosterol synthesis, were up-regulated. The genes encoding glutathione S-transferase, (GST), which has antioxidant activity and ABC transporters which have an efflux function, were also up-regulated.

CONCLUSION

These results show that the response of Vm to Sy Hhs.015 exposure is a complicated and highly regulated process, and provide a theoretical basis for both clarifying the biocontrol mechanism of Sy Hhs.015 and the response of Vm to stress.

摘要

背景

苹果树腐烂病是由苹果黑腐皮壳菌(Vm)引起的毁灭性枝干病害。内生放线菌杨树小菇(Sy Hhs.015)能有效抑制 Vm 的生长。为了揭示 Vm 对 Sy Hhs.015 响应的机制,本研究采用 RNA-seq 技术分析了 Vm 的转录组。

结果

与对照组中正常生长的 Vm 相比,Sy Hhs.015 处理组中有 1476 个基因显著差异表达,其中 851 个基因上调,625 个基因下调。对差异表达基因(DEGs)的基因功能和通路分析表明,Sy Hhs.015 影响了 Vm 用于能量产生的碳水化合物代谢途径。约 82%的糖苷水解酶基因下调,包括 3 个果胶酶基因(PGs),它们是关键的致病因子。Vm 的细胞壁结构被 Sy Hhs.015 破坏,细胞壁相关基因下调。过氧化物酶体相关基因中,编码过氧化氢酶(CAT)和超氧化物歧化酶(SOD)以清除活性氧(ROS)的基因,以及编码与脂肪酸β-氧化有关的 AMACR 和 ACAA1 的基因下调。乙醛酸循环的关键基因 MS 和 ICL 也下调。Vm 对 Sy Hhs.015 暴露的应激反应增加了氨基酸代谢以合成所需的含氮化合物,而参与三羧酸循环的α-酮酸可通过脱氨或转氨作用产生能量。与细胞壁葡聚糖合成有关的视黄醇脱氢酶和与细胞膜麦角固醇合成有关的甾醇 24-C-甲基转移酶上调。具有抗氧化活性的谷胱甘肽 S-转移酶(GST)和具有外排功能的 ABC 转运蛋白的基因也上调。

结论

这些结果表明,Vm 对 Sy Hhs.015 暴露的反应是一个复杂而高度调控的过程,为阐明 Sy Hhs.015 的生物防治机制和 Vm 对胁迫的反应提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/59f17a35fc5e/12866_2018_1225_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/a7e2dd0dfb33/12866_2018_1225_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/0a2c6a7b13ef/12866_2018_1225_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/1eb6a6c963bd/12866_2018_1225_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/f755f58687b7/12866_2018_1225_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/498acc9a4e06/12866_2018_1225_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/07d350e04e21/12866_2018_1225_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/0a82612cbc94/12866_2018_1225_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/e1533d00c5fd/12866_2018_1225_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/59f17a35fc5e/12866_2018_1225_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/a7e2dd0dfb33/12866_2018_1225_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/0a2c6a7b13ef/12866_2018_1225_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/1eb6a6c963bd/12866_2018_1225_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/f755f58687b7/12866_2018_1225_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/498acc9a4e06/12866_2018_1225_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/07d350e04e21/12866_2018_1225_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/0a82612cbc94/12866_2018_1225_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/e1533d00c5fd/12866_2018_1225_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b606/6106759/59f17a35fc5e/12866_2018_1225_Fig9_HTML.jpg

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