Andrew Smith ’17

Project TitleThe Length of Antisense RNA Indirectly Inhibits Translation of Beta-Galactosidase and Urease Enzymes
Mentor – Gerald Goldstein

Antisense RNA molecules in bacteria cause inhibition of translation of specific mRNA molecules and rapid destruction of the resulting double stranded RNAs by specific double stranded RNase enzymes. Antisense RNA therapy has been used successfully in the field of oncology to inhibit the synthesis of cell growth factors, growth factor receptors and proteins responsible for the invasive potential of tumor cells. Some antisense RNA molecules are short in length, 100 nucleotides, while other antisense RNA molecules are much larger. Some antisense RNA molecules are complementary to the 5’ end of the target mRNA molecule, the 3’ end of the target mRNA molecule, or the entire length of the mRNA molecule. We investigated the effectiveness of different lengths of antisense RNA molecules targeted against the 3’ end of the mRNA molecules for E. coli beta-galactosidase and Proteus vulgaris urease enzymes. Each of the antisense RNA molecules was complementary to the Shine-Dalgarno sequence, the initiation codon for translation, and various lengths of their respective mRNAs. The shortest antisense RNA molecule for beta-galactosidase, 76 RNA nucleotides in length, and for urease, 51 RNA nucleotides in length, inhibited synthesis of their respective enzymes 61% and 45%. The longest antisense RNA molecule for beta-galactosidase, 210 RNA nucleotides, and for urease, 226 RNA nucleotides, inhibited synthesis of their respective enzymes 0% and 20%. These results suggest that for these specific enzymes in these specific bacteria, the shorter the length the antisense RNA molecule was, the greater was the inhibition of enzyme synthesis.