Search bioRxiv⌕ Search

Biology subjects

Nicholson, L. S.

Publications and source records attributed to Nicholson, L. S..

2 recordsLinked to original sources

Establishing benchmarks for quantitative mapping of m6A by Nanopore Direct RNA Sequencing

Nanopore direct RNA sequencing (DRS) coupled with Dorado modification-aware basecalling enables mapping of epitranscriptomic modifications including N6-methyladenosine (m6A) at the level of individual RNAs. However, the sensitivity, specificity, and reproducibility of this method remain unclear and have only recently begun to be addressed through systematic benchmarking studies. Here, we aimed to establish a best-practice workflow for DRS-based epitranscriptomic analyses. Specifically, we evaluated multiple Dorado versions and models using RNA isolated from primary cells and unmodified in vitro transcribed RNAs. We further utilized an m6A methyltransferase inhibitor as a specificity control. We established that stringent filtering is necessary to reduce false-positive calls and found that Dorado predictions captured an increasing proportion of GLORI sites detected at high m6A/A proportions. Further, by applying DRS to human primary fibroblasts and HD10.6 neurons, we detected cell type-specific differences in the predicted m6A/A proportions at conserved sites. Our study thus presents the first systematic comparison of Dorado and GLORI from the same input RNA and expands characterization of the m6A epitranscriptome to fibroblasts and neurons.

bioinformatics↗

FTO depletion does not alter m6A stoichiometry in AML mRNA: a reassessment using direct RNA nanopore sequencing

The RNA demethylase FTO has been proposed to promote acute myeloid leukemia (AML) by demethylating N6-methyladenosine (m6A) from oncogenic transcripts, especially MYC. However, the evidence that supports the idea that FTO demethylates m6A in AML relies on methods that are non-quantitative and unable to reveal m6A stoichiometry changes before or after FTO depletion. To directly test whether FTO regulates m6A in mRNA, we employed Oxford Nanopore direct RNA sequencing to map and quantify m6A at single-nucleotide resolution. We find that the stoichiometry of m6A sites throughout the transcriptome and especially at MYC-specific sites are unaffected despite depletion of FTO activity by knockout, knockdown, or pharmacologic inhibition. This pattern was seen in AML cell lines MONOMAC-6 and MOLM-13, as well as in the non-AML cell line HEK293T. We also find that the anti-leukemia effect of the small-molecule FTO inhibitor FB23-2 is not due to FTO inhibition since it remains cytotoxic to FTO-deficient cells. Instead of regulating m6A, we find that FTO depletion markedly increases N6,2-O-dimethyladenosine (m6Am) in snRNAs, consistent with m6Am in snRNA being a target of FTO. Overall, our findings do not support an m6A eraser role for FTO in AML cell lines under the conditions tested, and they suggest that the reported demethylation functions of FTO on m6A should be reinvestigated using quantitative m6A mapping methods.

molecular biology↗