m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00608		[1], [2], [3]
m⁶A modification MIR320A MIR320A METTL3 Methylation : m⁶A sites Indirect Inhibition RNA modification NANOG NANOG METTL1 Methylation : modification sites
m6A Regulator	Methyltransferase-like 3 (METTL3)	WRITER	Regulator Info
m6A Target	hsa-mir-320a		Targert Gene
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type	RNA modification (RNAMod) >> N7-methylguanosine (m7G)
Epigenetic Regulator	Methyltransferase-like protein 1 (METTL1)	WRITER	View Details
Regulated Target	Homeobox protein NANOG (NANOG)		View Details
Crosstalk Relationship	m6A → m7G	Inhibition
Crosstalk Mechanism	m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary	METTL3 interacts with hsa-mir-320a, increasing its m6A level and inhibiting its physical interaction with Homeobox protein NANOG (NANOG), which was regulated by METTL1-mediated m7G modification.
In-vitro Model	iPSC (Mouse induced pluripotent stem cells (iPSCs))

References

Ref 1	METTL1-mediated m(7)G methylation maintains pluripotency in human stem cells and limits mesoderm differentiation and vascular development. Stem Cell Res Ther. 2020 Jul 22;11(1):306. doi: 10.1186/s13287-020-01814-4.
Ref 2	m(6)A Methylation of Precursor-miR-320/RUNX2 Controls Osteogenic Potential of Bone Marrow-Derived Mesenchymal Stem Cells. Mol Ther Nucleic Acids. 2020 Mar 6;19:421-436. doi: 10.1016/j.omtn.2019.12.001. Epub 2019 Dec 12.
Ref 3	MiR-320a was highly expressed in postmenopausal osteoporosis and acts as a negative regulator in MC3T3E1 cells by reducing MAP9 and inhibiting PI3K/AKT signaling pathway. Exp Mol Pathol. 2019 Oct;110:104282. doi: 10.1016/j.yexmp.2019.104282. Epub 2019 Jul 10.