Elevated WTAP promotes hyperinflammation by increasing m6A modification in inflammatory disease models.

Emerging evidence has linked the dysregulation of N6-methyladenosine (m6A) modification to inflammation and inflammatory diseases, but the underlying mechanism still needs investigation. Here, we found that high levels of m6A modification in a variety of hyperinflammatory states are p65-dependent because Wilms tumor 1-associated protein (WTAP), a key component of the "writer" complex, is transcriptionally regulated by p65, and its overexpression can lead to increased levels of m6A modification. Mechanistically, upregulated WTAP is more prone to phase separation to facilitate the aggregation of the writer complex to nuclear speckles and the deposition of m6A marks on transcriptionally active inflammatory transcripts, thereby accelerating the proinflammatory response.

Systematic calibration of epitranscriptomic maps using a synthetic modification-free RNA library.

Recent years have witnessed rapid progress in the field of epitranscriptomics. Functional interpretation of the epitranscriptome relies on sequencing technologies that determine the location and stoichiometry of various RNA modifications. However, contradictory results have been reported among studies, bringing the biological impacts of certain RNA modifications into doubt.

The Impact of Microbiome and Microbiota-Derived Sodium Butyrate on Transcriptome and Metabolome Revealed by Multi-Omics Analysis.

The host microbiome plays an important role in regulating physiology through microbiota-derived metabolites during host-microbiome interactions. However, molecular mechanism underly host-microbiome interactions remains to be explored. In this study, we used as the model to investigate the influence of microbiome and microbiota-derived metabolite sodium butyrate on host transcriptome and metabolome.