m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT00036
|
[1] | |||
.png)
.png)
 : m6A sites
Indirect
Enhancement
RNA modification
TRR-CCG1-1
TRR-CCG1-1
TRMT10A
Methylation
 : modification sites
|
|||||
| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | YTH domain-containing family protein 2 (YTHDF2) | READER | |||
| m6A Target | Forkhead box protein D1 (FOXD1) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | RNA modification (RNAMod) >> N1-methylguanosine (m1G) | ||||
| Epigenetic Regulator | tRNA methyltransferase 10 homolog A (TRMT10A) | WRITER | View Details | ||
| Regulated Target | tRNA-Arg (anticodon CCG) 1-1 (TRR-CCG1-1) | View Details | |||
| Crosstalk Relationship | m1G → m6A | Enhancement | |||
| Crosstalk Mechanism | RNA modification indirectly impacts m6A modification through downstream signaling pathways | ||||
| Crosstalk Summary | TRMT10A ablation not only leads to decreased m1G in tRNA (tRNAGln (TTG); TRNA-Arg (anticodon CCG) 1-1 (TRR-CCG1-1) and tRNAThr (CGT)) but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs (MYC; Forkhead box protein D1 (FOXD1) and AUPKAIP1) have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2. | ||||
| Pathway Response | RNA degradation | hsa03018 | |||
| Cell Process | mRNA decay | ||||