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Ren, Z.-H.

Publications and source records attributed to Ren, Z.-H..

2 recordsLinked to original sources

Deciphering the epitranscriptomic code of RNA degradation with nanopore direct RNA sequencing

The precise regulation of RNA degradation is crucial for gene expression homeostasis, yet how multiple molecular features coordinate on a single transcript remains poorly understood. Here, we use nanopore direct RNA sequencing (DRS) to simultaneously track alternative isoforms, m6A modifications, and poly(A) tail dynamics at single-molecule resolution during a time course of RNA decay. We show that m6A regulates RNA degradation in a stoichiometry-dependent manner, where modification levels quantitatively modulate decay kinetics. Mechanistically, m6A is functionally coupled to deadenylation, promoting accelerated poly(A) tail shortening and coordinated RNA turnover. At the isoform level, we identify regional m6A clusters (RMCs) as structural elements that associate with isoform-selective degradation and remodel protein-coding potential. Furthermore, transcript splicing architecture is associated with distinct m6A deposition patterns, suggesting that gene structure encodes RNA decay kinetics through m6A-mediated regulation. A machine learning model integrating these multi-modal features highlights the central contribution of m6A and deadenylation in shaping RNA decay, while revealing substantial regulatory heterogeneity across transcripts. Collectively, our study deciphers the multi-layered, cooperative principles of RNA degradation and provides an epitranscriptomic perspective for understanding how RNA fate is encoded at the single-molecule resolution.

bioinformatics↗

Single-Cell Multi-Omics Dissects Transcript Isoform and Immune Repertoire Dynamics in Human Immunosenescence

Immunosenescence, a major hallmark of systemic aging, refers to the progressive functional decline of the immune system. This decline not only compromises host defense and immunological memory but also fuels chronic inflammation and tissue degeneration (collectively known as inflammaging). While single-cell RNA sequencing (scRNA-seq) has revealed transcriptomic alterations in immune aging, analyses restricted to transcript abundance fail to capture deeper regulatory layers, such as transcript isoform diversity and the remodeling of immune receptor repertoires. To address this, we present the human peripheral immune single-cell multi-omics atlas that integrates gene expression, transcript isoforms diversity, and immune receptor repertoires. By combining single-cell full-length transcriptome sequencing (scCycloneSEQ), short-read scRNA-seq, and single-cell immune receptor sequencing (scTCR/BCR-seq), we systematically profiled peripheral blood mononuclear cells (PBMCs) from healthy young and elderly donors. Our analyses uncovered extensive age-related remodeling of immune cell composition, functional states, and TCR/BCR diversity. Notably, we identified in CD4 effector memory T cells exhibited widespread differential isoform usage (DIU), 3'UTR length variation, and a marked reshaping of cytotoxic T lymphocyte (CTL) clonotypes--all closely associated with aging-related inflammation and cellular senescence. This multi-omics atlas delineates key molecular features of immunosenescence and provides a high-resolution resource for deciphering the regulatory architecture underlying immune aging.

immunology↗