Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05653
[1]
m6A modification MALAT1 MALAT1 CYFIP2 : m6A sites Direct Enhancement Non-coding RNA Malat1 Regulated Target  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Cytoplasmic FMR1-interacting protein 2 (CYFIP2) READER
m6A Target Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) LncRNA View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary RNA immunoprecipitation and mass spectrometry revealed 12 new synapse-specific learning-induced m6A readers in the mPFC of male C57/BL6 mice, with m6A-modified Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) binding to a subset of these, including CYFIP2 and DPYSL2. In addition, a cell type- and synapse-specific, and state-dependent, reduction of m6A on Malat1 impairs fear-extinction memory; an effect that likely occurs through a disruption in the interaction between Malat1 and DPYSL2 and an associated decrease in dendritic spine formation.
In-vivo Model Adult, male C57BL/6J mice (9-10 weeks old, 20-25 g) supplied from the Animal Resources Center were used for experiments. Mice were housed 4 animals per cage on a 12 h light:dark cycle (lights on 0700 h) in a humidity- and temperature-controlled vivarium, with rodent chow and water provided ad libitum.
References
Ref 1 Synapse-Enriched m(6)A-Modified Malat1 Interacts with the Novel m(6)A Reader, DPYSL2, and Is Required for Fear-Extinction Memory. J Neurosci. 2023 Oct 25;43(43):7084-7100. doi: 10.1523/JNEUROSCI.0943-23.2023. Epub 2023 Sep 5.