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Abstract Several studies have now described instances where G-rich sequences in promoters and enhancers regulate gene expression through forming G-quadruplex (G4) structures. Relatedly, our group recently identified 301 long genomic stretches significantly enriched for minimal G4 motifs (LG4s) in humans and found the majority of these overlap annotated enhancers, and furthermore, that the promoters regulated by these LG4 enhancers are similarly enriched with G4-capable sequences. While the generally accepted model for enhancer:promoter specificity maintains that interactions are dictated by enhancer- and promoter-bound transcriptional activator proteins, the current study tested an alternative hypothesis: that LG4 enhancers interact with cognate promoters via a direct G4:G4 DNA-based mechanism. This work establishes the nuclear proximity of LG4 enhancer:promoter pairs, biochemically demonstrates the ability of individual LG4 single-stranded DNAs (ssDNAs) to directly interact target promoter ssDNAs, and confirms that these interactions, as well as the ability of LG4 enhancers to activate target promoters in culture, are mediated by G4 DNA. 

Y RNAs are a poorly-studied class of small non-coding RNAs (sncRNAs) which have previously been implicated in the pathogenesis of different human diseases, including cardiac and autoimmune conditions, as well as certain cancers. In recent years, however, multiple studies have reported correlations between Y RNA expressions and disease outcomes in viral infections (e.g., IAV, HIV, HPV, and SARS-CoV-2) as well as potential mechanistic roles that Y RNAs may play in host anti-viral defense. These studies suggest that Y RNAs may be associated with upregulation of viral defense proteins as well as altered cell-cell communication during viral infections. In this review, current literature detailing Y RNA effects on human viral infection will be summarized and future directions in the study of these relationships discussed.