Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05718
[1]
m6A modification GAS5 GAS5 YTHDF2 : m6A sites Direct Inhibition Non-coding RNA GAS5 DRP1  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator YTH domain-containing family protein 2 (YTHDF2) READER
m6A Target Growth arrest specific 5 (GAS5)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Growth arrest specific 5 (GAS5) LncRNA View Details
Regulated Target Dynamin-1-like protein (DRP1) View Details
Crosstalk Relationship m6A  →  ncRNA Inhibition
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary METTL3 mediated m6A methylation of LncRNA-Growth arrest specific 5 (GAS5) via an YTHDF2-dependent manner. METTL3 boosts mitochondrial fission and induces cardiac fibrosis by enhancing LncRNA GAS5 methylation. Overexpression of GAS5 suppressed Dynamin-1-like protein (DRP1)-mediated mitochondrial fission, inhibiting cardiac fibroblast proliferation and migration.
Responsed Disease Vascular disorders of the liver ICD-11: DB98.8
Cell Process Cell proliferation
Cell migration
In-vitro Model
NIH 3T3 Normal Mus musculus CVCL_0594
In-vivo Model The in vivo assay was approved by the Animal Care and Use Committee of Anhui Medical University. And all experimental procedures and animal care were in accordance with the institutional ethics guidelines for animal experiments. The C57BL/6 mice (male, 8-10 weeks old) were housed (six per cage) in a specific and opportunistic pathogen-free facility and maintained on a 12-hlight-dark cycle with casually access to food and water. Detailed descriptions of the cell culture, cardiac fibrosis model, and treatment with lentiviral, were given in the Supplementary methods online.
References
Ref 1 METTL3 boosts mitochondrial fission and induces cardiac fibrosis by enhancing LncRNA GAS5 methylation. Pharmacol Res. 2023 Aug;194:106840. doi: 10.1016/j.phrs.2023.106840. Epub 2023 Jun 26.