AbstractStudies have shown that the m6A reader primarily affects genes expression by participating in the regulation of mRNA localization, splicing, degradation, translation, and other metabolic processes. Previously, we discovered that the apple (Malus domestica) m6A reader MhYTP2 bound with and destabilized m6A-modifiedMdMLO19mRNA. In addition, it enhanced the translation efficiency of m6A-modified mRNA ofMdGDH1L, encoding a glutamate dehydrogenase, which confers resistance to powdery mildew. In this study, we report the function of MhYTP2 in the regulation of resistance to low nitrogen (N). The overexpression ofMhYTP2enhances the resistance of apple to low N. We show that MhYTP2 binds with and stabilizes the mRNAs ofMdALN, which participates in the allantoin catabolic process and cellular response to N starvation in apple;MdPIDL, which participates in root hair elongation;MdTTG1, which is involved in the differentiation process of trichomes; andMdATG8A, which is a core participant in the regulation of autophagy. In addition, MhYTP2 accelerates the degradation ofMdRHD3mRNA, which regulates root development. RNA immunoprecipitation-seq and electrophoretic mobility shift assays show that the mRNAs ofMdALN,MdATG8A,MdPIDL,MdTTG1, andMdRHD3are the direct targets of MhYTP2. Overexpressing or knocking down the above genes inMhYTP2overexpressing plants dismisses the function of MhYTP2 under low N, suggesting the role of MhYTP2 is dependent on those genes. Together, these results demonstrate that MhYTP2 enhances the resistance of apple to N deficiency by affecting the stability of the bound mRNAs.