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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE285757 | GEO | 2026/03/17

REPOSITORIES: GEO

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Ftsj1 deficiency influences diverse ncRNA networks in murine organs (miRNAs)

Project description: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 miRNA-seq data used in our study.

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Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.

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Increased serum miR-193a-5p during non-alcoholic fatty liver disease progression: diagnostic and mechanistic relevance

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The ribose methylation enzyme FTSJ1 has a conserved role in neuron morphology and learning performance

Project description:FTSJ1 is a conserved human 2’-O-methyltransferase (Nm-MTase) that modifies several transfer RNAs (tRNAs) at position 32 and the wobble position 34 in the AntiCodon Loop (ACL). Its loss of function has been linked to Non-Syndromic X-Linked Intellectual Disability (NSXLID), and more recently to cancers. However, the molecular mechanisms underlying these pathologies are currently unclear. Here we report a novel FTSJ1 pathogenic variant from a NSXLID patient. Using blood cells derived from this patient and other affected individuals carrying FTSJ1 mutations, we performed an unbiased and comprehensive RiboMethSeq analysis to map the ribose methylation (Nm) on all tRNAs and identify novel targets. In addition, we performed a transcriptome analysis in these cells and found that several genes previously associated with intellectual disability and cancers were deregulated. We also found changes in the miRNA population that suggest potential cross-regulation of some miRNAs with these key mRNA targets. Finally, we show that differentiation of FTSJ1-depleted human neuronal progenitor cells (NPC) into neurons displays long and thin spine neurites compared to control cells. These defects are also observed in Drosophila and are associated with long term memory deficit in this organism. Altogether, our study adds insight into FTSJ1 pathologies in human by the identification of novel FTSJ1 targets and the defect in neuron morphology.

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