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脾脏 mRNA mA 甲基化的表观转录组分析揭示了宿主对疟原虫感染的反应途径。

Epitranscriptome profiling of spleen mRNA mA methylation reveals pathways of host responses to malaria parasite infection.

机构信息

School of Life Sciences, South China Normal University, Guangzhou, China.

Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, United States.

出版信息

Front Immunol. 2022 Sep 20;13:998756. doi: 10.3389/fimmu.2022.998756. eCollection 2022.

DOI:10.3389/fimmu.2022.998756
PMID:36203583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9531237/
Abstract

-Methyladenosine (mA), the most abundant mammalian mRNA modification, has been reported to modulate various viral infections. Although it has been confirmed that RNA modifications can also modulate the replication and development of different parasites, the role of the RNA epitranscriptome in the regulation of host response post parasite infection remains to be elucidated. Here we report host spleen mA epitranscriptome landscapes induced by different strains of the malaria parasite . We found that malaria parasite infection dramatically changes host spleen mA mRNA modification and gene expression. Additionally, malaria parasite infection reprograms host immune response pathways by regulating the mA modification enzymes. Collectively, our study is the first characterization of host spleen mA methylome triggered by malaria parasite infections, and our data identify mA modifications as significant transcriptome-wide marks during host-parasite interactions. We demonstrate that host mRNA methylation machinery can sense and respond to malaria parasite infections, and provide new insights into epitranscriptomic mechanisms underlying parasite-induced pathogenesis.

摘要
  • 甲基腺苷（mA）是哺乳动物 mRNA 中最丰富的修饰物，已有报道称其可调节多种病毒感染。尽管已经证实 RNA 修饰也可以调节不同寄生虫的复制和发育，但宿主对寄生虫感染后的反应中 RNA 表转录组的作用仍有待阐明。在这里，我们报告了疟原虫不同株系诱导的宿主脾 mA 表转录组图谱。我们发现疟疾寄生虫感染显著改变了宿主脾 mA mRNA 修饰和基因表达。此外，疟疾寄生虫感染通过调节 mA 修饰酶来重新编程宿主免疫反应途径。总的来说，我们的研究首次描述了疟原虫感染引发的宿主脾 mA 甲基组，我们的数据表明 mA 修饰是宿主-寄生虫相互作用过程中转录组的重要标记。我们证明了宿主 mRNA 甲基化机制可以感知和响应疟原虫感染，并为寄生虫诱导发病机制的表转录组机制提供了新的见解。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/a532425666fa/fimmu-13-998756-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/948c47404b2a/fimmu-13-998756-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/a16adc3d2955/fimmu-13-998756-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/169a97db3122/fimmu-13-998756-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/c1b024320f86/fimmu-13-998756-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/a532425666fa/fimmu-13-998756-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/948c47404b2a/fimmu-13-998756-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/a16adc3d2955/fimmu-13-998756-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/169a97db3122/fimmu-13-998756-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/c1b024320f86/fimmu-13-998756-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3a/9531237/a532425666fa/fimmu-13-998756-g005.jpg

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Plasmodium falciparum YTH2 Domain Binds to m6A-Containing mRNA and Regulates Translation.恶性疟原虫YTH2结构域与含m6A的mRNA结合并调节翻译。
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