Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00067
[1]
RNA modification SOX9 SOX9 NSUN4 Methylation : modification sites Direct Enhancement m6A modification SOX9 SOX9 METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Transcription factor SOX-9 (SOX9)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator 5-methylcytosine rRNA methyltransferase NSUN4 (NSUN4) WRITER View Details
Regulated Target Transcription factor SOX-9 (SOX9) View Details
Crosstalk Relationship m5C  →  m6A Enhancement
Crosstalk Mechanism RNA modification directly impacts m6A modification through recruiting m6A regulator and targeting the shared RNA
Crosstalk Summary BMSCs overexpressing METTL3 and NSUN4 can promote the repair of cartilage defects in vivo. m5C and m6A co-regulate the translation of Transcription factor SOX-9 (SOX9) in a YTHDF2-dependent manner during the chondrogenic differentiation of BMSCs, which provides a therapeutic target for clinical implications.
Cell Process Cell differentiation
In-vivo Model The rats were anaesthetized via strictly aseptic techniques during surgery. The knee joint was opened laterally by dislocating the patellar tendon, and a full thickness osteochondral defect (3-mm in diameter) was created in the trochlear groove of the femur. Then, approximately 107BMSCs were mixed with 1 ml hydrogel matrix (Coring, Cat#354250) and were injected into the defect.
References
Ref 1 Nsun4 and Mettl3 mediated translational reprogramming of Sox9 promotes BMSC chondrogenic differentiation. Commun Biol. 2022 May 25;5(1):495. doi: 10.1038/s42003-022-03420-x.