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METTL14 和 FTO 通过影响 miR-30a-5p 的成熟来调节 mA 修饰，从而调节 PCV2 的复制。

METTL14 and FTO mediated mA modification regulate PCV2 replication by affecting miR-30a-5p maturity.

机构信息

Shandong Key Laboratory of Animal Disease Control and Breeding, Institute of Animal Science and Veterinary Medicine, Shandong Academy of Agricultural Sciences, jinan, P. R. China.

College of Life Sciences, Shandong Normal University, Jinan, China.

出版信息

Virulence. 2023 Dec;14(1):2232910. doi: 10.1080/21505594.2023.2232910.

DOI:10.1080/21505594.2023.2232910
PMID:37418592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10332184/
Abstract

The epigenetic modification of the N6-methyladenosine (mA) methylation plays an important role in virus infection and replication. However, its role in Porcine circovirus type 2 (PCV2) replication has not been well studied. Here, we demonstrated that mA modifications are increased in PK-15 cells after PCV2 infection. In particular, PCV2 infection could increase the expression of methyltransferase METTL14 and demethylase FTO. Moreover, interfering with METTL14 accumulation reduced the mA methylation level and virus reproduction, whereas depleting the FTO demethylase enhanced the mA methylation level and stimulated virus reproduction. Besides, we showed that METTL14 and FTO regulate PCV2 replication by affecting the process of miRNA maturity, especially the miRNA-30a-5p. Taken together, our results demonstrated that the mA modification positively affects PCV2 replication and the role of mA modification in the replication mechanism of the PCV2 virus provides a new idea for the prevention and control of the PCV2.

摘要

N6-甲基腺苷（m6A）甲基化的表观遗传修饰在病毒感染和复制中发挥着重要作用。然而，其在猪圆环病毒 2 型（PCV2）复制中的作用尚未得到充分研究。在这里，我们证明了 PCV2 感染后 PK-15 细胞中的 mA 修饰增加。具体而言，PCV2 感染可以增加甲基转移酶 METTL14 和去甲基酶 FTO 的表达。此外，干扰 METTL14 的积累会降低 mA 甲基化水平并抑制病毒复制，而耗尽 FTO 去甲基酶则会增加 mA 甲基化水平并刺激病毒复制。此外，我们还表明，METTL14 和 FTO 通过影响 miRNA 成熟过程（特别是 miRNA-30a-5p）来调节 PCV2 的复制。总之，我们的研究结果表明，mA 修饰正向影响 PCV2 的复制，mA 修饰在 PCV2 病毒复制机制中的作用为防控 PCV2 提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/63e9d7d4c004/KVIR_A_2232910_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/67c40218bca4/KVIR_A_2232910_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/98c04a490d00/KVIR_A_2232910_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/52e12c13f0d7/KVIR_A_2232910_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/7cd6d6e4908f/KVIR_A_2232910_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/eba3b26484cf/KVIR_A_2232910_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/63e9d7d4c004/KVIR_A_2232910_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/67c40218bca4/KVIR_A_2232910_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/98c04a490d00/KVIR_A_2232910_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/52e12c13f0d7/KVIR_A_2232910_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/7cd6d6e4908f/KVIR_A_2232910_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/eba3b26484cf/KVIR_A_2232910_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89c7/10332184/63e9d7d4c004/KVIR_A_2232910_F0006_OC.jpg

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