🧬 PubMed RNA Editing Daily Digest

C-to-U editing is a critical post-transcriptional modification process in plant mitochondrial RNAs, involving the conversion of specific cytidine (C) residues to uridine (U). Pentatricopeptide repeat (PPR) proteins serve as site-specific recognition factors in this process. Although certain DYW-type PPR proteins (DYW-PPR) are known to participate in the post-transcriptional processing of mitochondrial RNAs, the functions of more than 60 DYW-PPR proteins in maize remain uncharacterized. In this study, we identify a novel DYW-PPR protein, DEK618, which is associated with defective kernel development and dwarfism in maize. A 254 bp insertion in the Dek618 gene disrupted protein expression and resulted in abnormal mitochondrial morphology. Loss of DEK618 function altered the editing efficiency at 88 C-to-U sites. Notably, editing at cob-298, ccmC-184, ccmB-428, and ccmFC-1219 was completely abolished in the dek618 mutant, likely due to impaired mitochondrial function affecting the assembly and activity of mitochondrial complex III. Furthermore, DEK618 was found to physically interact with ZmMORF1 and ZmMORF8, suggesting that these proteins collaborate to facilitate C-to-U RNA editing as part of a complex within mitochondria.

Cervical cancer (CC) remains one of the most prevalent gynecological malignancies worldwide, with patients diagnosed at advanced stages often facing poor prognoses due to the lack of effective therapeutic options. ADARB1 (Adenosine Deaminase Acting on RNA 1), an RNA-editing enzyme, has been implicated in the pathogenesis of various cancers; however, its functional role in cervical cancer remains largely unexplored. In this study, we observed a significant downregulation of ADARB1 expression in both cervical cancer tissues and cell lines, which was associated with unfavorable clinical outcomes. Functional assays revealed that ADARB1 overexpression markedly inhibited the proliferation, migration, invasion, and glycolytic activity of cervical cancer cells, whereas ADARB1 knockdown exerted the opposite effects. Mechanistically, we found that ADARB1 mRNA binds to HMGB1 (High Mobility Group Box 1) protein and regulates its expression via the ubiquitin-proteasome pathway, thereby modulating the malignant phenotype of cervical cancer. Notably, ectopic expression of HMGB1 partially reversed the suppressive effects of ADARB1 on cell proliferation and glycolysis. Further investigation revealed that HMGB1 interacts with PFKFB3 (6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase 3), a key regulatory enzyme in glycolysis, and modulates its protein stability, suggesting the presence of a critical HMGB1/PFKFB3 signaling axis in cancer metabolism. ADARB1 exerts its anti-tumor effects primarily through the HMGB1/PFKFB3 pathway. Collectively, these findings identify ADARB1 as a novel tumor suppressor in cervical cancer and a promising therapeutic target for clinical intervention.

Functional exhaustion and inefficient tumor infiltration rates limit the effectiveness of natural killer (NK) cell-based cancer immunotherapy. Although the role of adenosine deaminase acting on RNA 1 (ADAR1) in immune cells and tumorigenesis is gradually gaining attention, its role in NK cells is elusive. In this study, we find that ADAR1 expression level is increased in peripheral blood (PB)-NK cells from patients with melanoma, concurrently exhibiting impaired tumor killing capacity. ADAR1-knockdown NK cells show enhanced antitumor activity in vitro and in vivo. Compared with ADAR1

To develop and evaluate a rapid, one-pot molecular assay for the detection of Treponema pallidum subspecies pallidum (TPA), addressing the limitations of current diagnostic methods influenced by sample type and pathogen load. A one-pot assay integrating recombinase polymerase amplification (RPA) and Cas13a-based collateral cleavage activity was established for isothermal detection of TPA. The assay targeted the tpp47/tp0574 gene and was validated using 186 clinical specimens, including whole blood, lesion exudate, and cerebrospinal fluid (CSF) samples. The one-pot RPA-Cas13a assay demonstrated high analytical sensitivity and specificity for TPA detection. Clinical sensitivities were 58.97% in whole blood, 84.21% in lesion exudate, and 57.14% in CSF, with 100% specificity across all sample types. This one-pot isothermal assay enables rapid and accurate detection of T. pallidum directly from diverse clinical samples. Its high specificity and field-friendly format make it a promising complementary tool to conventional diagnostic approaches, particularly for point-of-care testing and screening in resource-limited or high-risk settings.

RNA editing introduces transcriptomic variation and may contribute to complex trait regulation. However, its genetic determination in pigs remains unclear. Here, using 5457 PigGTEx RNA-seq samples across 34 porcine tissues, we construct a comprehensive RNA editome and map 49 614 cis-editing quantitative trait loci (edQTLs). These edQTLs define a distinct regulatory layer, with over 32% acting independently of expression or splicing QTLs (eQTLs/sQTLs). Crucially, edQTLs are significantly enriched in GWAS loci for 33 complex traits and show a superior contribution to heritability over eQTLs/sQTLs in some traits like growth and reproduction. Colocalization analyses pinpoint diverse causal mechanisms, revealing both edQTL-specific effects (e.g., ERCC5) and coordinated events where single variants pleiotropically modulate RNA editing, splicing, and gene expression. Human-pig comparative analysis identifies hundreds of evolutionarily conserved editing events linked to fundamental neurological pathways. This study provides the first comprehensive multi-tissue porcine RNA editome and edQTL map, establishing RNA editing as a key mechanism linking genetic variation to phenotypic diversity in a major agricultural species and offering a valuable resource for future functional genomics research.