Bridge Nucleic Acid/DNA Gapmers as Potential Inhibitors of Bacterial Gene Expression by Multiple Antisense Mechanisms: An In Vitro Study

桥接核酸/DNA Gapmers作为多种反义机制抑制细菌基因表达的潜在抑制剂:一项体外研究

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Abstract

Antisense inhibition of gene expression is usually achieved using nuclease-resistant oligonucleotide analogs that promote mRNA degradation through RNase H or RNase P, or by steric hindrance of translation. Bridge nucleic acids (BNAs) are nucleotide analogs available in a few chemical variants. We evaluated gapmers composed of an oligodeoxynucleotide flanked by BNA residues in a BNA(5)-DNA(8)-BNA(4) configuration, using the available variants: the original locked nucleic acid (LNA; 2'-O,4'-methylene bridge), cET (2'-O,4'-ethyl bridge), cMOE (2'-O,4'-methoxyethyl bridge), and BNANC (2'-O,4'-aminomethylene bridge). These gapmers were tested in vitro for their ability to induce cleavage of the model aac(6')-Ib mRNA. All gapmers complementary to a previously identified region suitable for interaction with antisense oligomers induced RNase H-mediated degradation. Instead, only the LNA-containing gapmer also elicited RNase P-dependent cleavage, demonstrating dual RNA- and DNA-mimicking capability. In vitro coupled transcription-translation assays using cell lysates or reconstituted systems confirmed inhibition of expression and ruled out steric hindrance as the mechanism. In contrast, gapmers targeting the ribosome-binding site strongly inhibited expression by steric hindrance. These findings demonstrate that LNA-containing gapmers can exert their effects through multiple mechanisms, depending on the targeted mRNA region, thereby supporting their potential for synergistic inhibition of gene expression.

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