Ftsj1 deficiency influences diverse ncRNA networks in murine organs (poly-A-seq and rRNA-depletion-seq)

Beyond the regulation of mRNAs by individual ncRNA types, such as miRNAs or lncRNAs, their interplay as so-called competitive endogenous RNAs (ceRNAs) appears to play a pivotal role in diseases. In our study we aimed to get a holistic understanding of the tRNA 2’O-methyltransferase FTSJ1 and its regulatory role in the context of cognitive disability. Here, we investigated the impact of Ftsj1 deficiency on ceRNA networks across different mouse organs. Our study underscores the critical role of organ-specific ceRNA networks, particularly in metabolic regulation, and emphasizes the need for cross-organ analyses to unravel the complexity of ceRNA-mediated gene regulation. Our findings reveal a prominent ceRNA network in the liver, mediated by four hub miRNAs (miR-378d, miR-3076-5p, miR-3474, and miR-296-3p) and enriched with acetyl CoA-related genes, including Acly, Acss2, and Mvk. These genes are integral to fatty acid metabolism, which is heavily disrupted in both liver and kidney. In contrast, brain tissues exhibited minimal changes, suggesting only a limited impact directly related to Ftsj1 in this organ. These results suggest that the cognitive disability associated with Ftsj1 is driven by metabolic and ceRNA crosstalk along the liver-brain and kidney-brain axes. This dataset comprises the poly-A and rRNA-depletion total RNA sequencing data used in our study for mRNAs and lncRNAs.