The study presents a novel method for mapping N6-methyladenosine (m6A) and N6,2'-O-dimethyladenosine (m6Am) at single-nucleotide resolution across the transcriptome. The method, called miCLIP, uses anti-m6A antibodies crosslinked to RNA via UV light, followed by reverse transcription, which induces specific mutational signatures at m6A and m6Am sites. These signatures enable precise identification of m6A and m6Am residues in human and mouse mRNA. The study also identifies snoRNAs as a novel class of m6A-containing non-coding RNAs. The research demonstrates that anti-m6A antibodies can induce specific mutational signatures, such as C→T transitions and truncations, which are used to map m6A and m6Am. These signatures are highly specific and allow for the identification of m6A and m6Am at single-nucleotide resolution. The study shows that m6A is enriched in specific motifs, such as DRACH, and that miCLIP can detect m6A in both coding and non-coding regions of mRNA. The study also reveals that m6A is often clustered in mRNAs, and that miCLIP can identify these clusters with high accuracy. Additionally, miCLIP can detect m6Am, a related modification found at the first nucleotide following the 7-methylguanosine cap of certain mRNAs. The method is validated using known m6A and m6Am sites, and it is shown to have high specificity and sensitivity. The study highlights the importance of m6A in mRNA regulation and its role in various biological processes. The development of miCLIP provides a powerful tool for studying m6A and m6Am across the transcriptome, enabling the identification of specific m6A and m6Am residues in a wide range of RNA species, including snoRNAs. The method is also applicable to other RNA modifications for which antibodies exist.The study presents a novel method for mapping N6-methyladenosine (m6A) and N6,2'-O-dimethyladenosine (m6Am) at single-nucleotide resolution across the transcriptome. The method, called miCLIP, uses anti-m6A antibodies crosslinked to RNA via UV light, followed by reverse transcription, which induces specific mutational signatures at m6A and m6Am sites. These signatures enable precise identification of m6A and m6Am residues in human and mouse mRNA. The study also identifies snoRNAs as a novel class of m6A-containing non-coding RNAs. The research demonstrates that anti-m6A antibodies can induce specific mutational signatures, such as C→T transitions and truncations, which are used to map m6A and m6Am. These signatures are highly specific and allow for the identification of m6A and m6Am at single-nucleotide resolution. The study shows that m6A is enriched in specific motifs, such as DRACH, and that miCLIP can detect m6A in both coding and non-coding regions of mRNA. The study also reveals that m6A is often clustered in mRNAs, and that miCLIP can identify these clusters with high accuracy. Additionally, miCLIP can detect m6Am, a related modification found at the first nucleotide following the 7-methylguanosine cap of certain mRNAs. The method is validated using known m6A and m6Am sites, and it is shown to have high specificity and sensitivity. The study highlights the importance of m6A in mRNA regulation and its role in various biological processes. The development of miCLIP provides a powerful tool for studying m6A and m6Am across the transcriptome, enabling the identification of specific m6A and m6Am residues in a wide range of RNA species, including snoRNAs. The method is also applicable to other RNA modifications for which antibodies exist.