Abstract
N[1]-methyladenine (m[1]A), a modification of transcripts, regulates mRNA structure and translation efficiency. In a recent issue of Nature, Sun et al. reported that m[1]A in CAG repeat RNA contributes to CAG repeat expansion-induced neurodegeneration in Caenorhabditis elegans and Drosophila through enhancing the ability of endogenous TDP-43 to partition into stress granules mediated by m[1]A. The study is especially important for revealing the pathological function of m[1]A in RNA and the pathological mechanisms of CAG repeat expansion-related neurodegenerative diseases.
