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A high-resolution RNA interaction atlas of Arabidopsis thaliana TUDOR STAPHYLOCOCCAL NUCLEASE 1 captured by in vivo iCLIP

ABSTRACT: RNA-binding proteins (RBPs) are key regulators of the RNA life cycle, exerting broad effects on plant physiology and development. Their function relies on direct RNA interactions, making the identification of in vivo targets and binding patterns critical for understanding their regulatory roles. Here, we characterize the RNA-binding landscape of the Arabidopsis thaliana RBP TUDOR STAPHYLOCOCCAL NUCLEASE 1 (TSN1), previously implicated in stress responses in plants. Using an adapted individual-nucleotide resolution crosslinking and immunoprecipitation (iCLIP2) approach, we mapped TSN1 binding sites across the transcriptome and identified 1,504 direct RNA targets, predominantly protein-coding transcripts. Motif analysis revealed three enriched consensus sequences: a U-rich motif, an A-rich motif and a G/U-rich motif. Functional enrichment analysis of TSN1 targets showed significant associations with core metabolic processes, including photosynthesis, as well as hormonal pathways involved in plant immunity responses. Together, these data provide a high-resolution map of TSN1–RNA interactions that serves as a resource to explore TSN1-dependent role in gene expression regulation in plants.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE337496 | GEO | 2026/07/30

REPOSITORIES: GEO

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Project description:BACKGROUND: Imbalances in cardiac branched-chain amino acid (BCAA) metabolism and mitochondrial homeostasis are implicated in the onset and development of heart failure. However, the mechanisms triggering the downregulation of cardiac BCAA metabolism in heart failure remain unclear. Here, we identify a novel role of RNA-binding protein GRSF1 (guanine-rich RNA sequence binding factor 1) in post-transcriptionally regulating cell-intrinsic BCAA metabolic pathways, ultimately contributing to the pathogenesis of heart failure.METHODS: We examined GRSF1 expression in the heart tissues of patients with dilated cardiomyopathy and generated mice with cardiomyocyte-specific deletion or overexpression of GRSF1 in vivo to investigate its role in heart failure. The effect of GRSF1 on BCAA homeostasis was assessed through untargeted and targeted metabolomics and mitochondrial function analysis. To elucidate the mechanisms underlying GRSF1-mediated metabolic regulation, we employed mice with cardiomyocyte-specific deletion of BCKDHB, and mice with cardiomyocyte-specific expression of GRSF1 lacking a quasi-RNA recognition motif. RESULTS: GRSF1 expression was significantly decreased in the hearts of patients with heart failure and failing murine hearts. Cardiomyocyte-specific GRSF1 deletion resulted in cardiac dysfunction, spontaneous progression to dilated cardiomyopathy, and heart failure, accompanied by increased cardiac hypertrophy and fibrosis. Conversely, GRSF1 overexpression attenuated cardiac remodeling and heart failure induced by transverse aortic constriction. Mechanistically, GRSF1 maintained BCAA homeostasis and mitochondrial function by directly interacting with the G-tracts in coding region of BCKDHB mRNA through a quasi-RNA recognition motif to promote the stability of BCKDHB mRNA at the post-transcriptional level, thereby increasing its protein expression. Functional recovery mediated by GRSF1 overexpression in cardiomyocytes was partially blocked upon cardiac-specific deletion of BCKDHB.  CONCLUSIONS: Our study identified GRSF1 as a cell-intrinsic metabolic checkpoint that maintains cardiac BCAA homeostasis by regulating BCKDHB mRNA turnover. Targeting GRSF1 may offer therapeutic benefits for heart failure and other cardiometabolic diseases requiring BCAA manipulation.

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A high-resolution RNA interaction atlas of Arabidopsis thaliana TUDOR STAPHYLOCOCCAL NUCLEASE 1 captured by in vivo iCLIP

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