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Enterovirus 71 structural viral protein 1 promotes the expression of PMP22 through m6A modification in mouse Schwann
Qiuyan Peng1, Guangming Liu2, Danping Zhu2
1Jinan University, #601, Huangpu Avenue West, Guangzhou 510632, Guangdong, PR China.
Purpose:
Enterovirus 71 (EV71) is one of the enteroviruses that causes hand-foot-and-mouth disease (HFMD). This study aims to investigate the role of EV71 structural viral protein 1 (VP1) in mouse Schwann cells.
Methods:
An EV71 VP1-expressing vector was generated and transfected into mouse Schwann cells (MSCs). Small interfering RNAs against methyltransferase-like protein 14 (METTL14) and YTH N6-Methyladenosine RNA Binding Protein 1 (YTHDF1) were used to knock down the expressions of METTL14 and YTHDF1 in MSCs to investigate their roles in peripheral myelin protein 22 (PMP22) expression. Real-time PCR and Western blot analysis were performed to determine the expressions of PMP22 and m6A modification-associated proteins.
Results:
EV71-VP1 over-expression significantly increased the expressions of transmethylase METTL3/14 and m6A methylation recognition protein YTHDC1 and YTHDF1/2/3 in MSCs. On the contrary, the level of demethylase FTO, but not ALKBH5, was obviously decreased in VP1-over-expressed MSCs. Furthermore, 3-DZA inhibited expressions of METTL3/14 and YTHDF1/2 in VP1-over-expressed MSCs, indicating METTL3/14 and YTHDF1/2 were the key m6A-modification-related genes regulated by VP1. In addition, deficiency of METTL14 or YTHDF1 contracted the up-regulation of PMP22 induced by VP1 overexpression in MSCs.
Conclusions:
VP1 up-regulated PMP22 via m6A modification in MSCs, which were mainly affected by METTL14 and YTHDF1.
Insights
Enterovirus 71 (EV71) structural protein 1 (VP1) increases peripheral myelin protein 22 (PMP22) in mouse Schwann cells. This occurs through N6-methyladenosine (m6A) modification, primarily involving METTL14 and YTHDF1.
Area of Science:
- Virology
- Molecular Biology
- Neuroscience
Background:
- Enterovirus 71 (EV71) is a significant cause of hand-foot-and-mouth disease (HFMD).
- Schwann cells are crucial for peripheral nerve myelination.
- The molecular mechanisms linking EV71 infection to Schwann cell dysfunction are not fully understood.
Purpose of the Study:
- To investigate the role of EV71 structural protein 1 (VP1) in mouse Schwann cells (MSCs).
- To elucidate the involvement of N6-methyladenosine (m6A) modification in EV71 VP1-mediated effects on PMP22 expression.
Main Methods:
- EV71 VP1 was overexpressed in MSCs using a viral vector.
- Knockdown of METTL14 and YTHDF1 was performed using small interfering RNAs.
- Gene and protein expression levels of PMP22 and m6A-associated factors were analyzed via real-time PCR and Western blot.
Main Results:
- EV71 VP1 overexpression upregulated key m6A methyltransferases (METTL3/14) and readers (YTHDC1, YTHDF1/2/3), while downregulating demethylase FTO.
- METTL14 and YTHDF1 were identified as critical mediators of VP1's effect.
- Deficiency in METTL14 or YTHDF1 attenuated the VP1-induced upregulation of PMP22.
Conclusions:
- EV71 VP1 upregulates PMP22 expression in mouse Schwann cells through m6A modification.
- METTL14 and YTHDF1 are key m6A-related proteins mediating this VP1-induced PMP22 upregulation.
