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Knockdown of METTL16 disrupts learning and memory by reducing the stability of MAT2A mRNA
Runjiao Zhang1,2, Yizhou Zhang1,2,3, Fangzhen Guo1,2
1Department of Anatomy, Hebei Medical University, 050017, Shijiazhuang, Hebei, China.
Abstract:
N6-methyladenosine (m6A) is abundant in the mammalian brain and is considered to have a wide range of effects on learning and memory. Here, we found that the upregulated methyltransferase-like protein 16 (METTL16) in the hippocampal tissues of Morris water maze (MWM)-trained mice contributed to improved memory formation and hippocampal synaptic plasticity. Mechanismly, METTL16 promoted the expression of methionine adenosyltransferase 2A (MAT2A) by the m6A methylation of the MAT2A mRNA-3'UTR-end to increase its stability, and this involved in improving hippocampal global m6A levels, plasticity of dendritic spine, learning and memory. This study provides a new perspective to explore the regulatory mechanisms of m6A for learning and memory.
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