Activation of alpha-toxin translation in Staphylococcus aureus by the trans-encoded antisense RNA, RNAIII.
The synthesis of virulence factors in Staphylococcus aureus is controlled by a regulatory RNA molecule, RNAIII, encoded by the agr locus. Transcription of genes coding for secreted toxins and enzymes is stimulated, while transcription of cell-surface protein genes is repressed by RNAIII. In the case of staphylococcal alpha-toxin, RNAIII also seems to stimulate translation by an independent mechanism. In this report we show that in a mutant lacking RNAIII the rate of alpha-toxin ( hla) production relative to the cellular concentration of hla mRNA was reduced 10-fold as compared with the wild-type strain. A 75% complementarity between the 5' end of RNAIII and the 5' untranslated region of the hla transcript suggests a direct interaction between the RNAs. A complex of RNAIII and hla mRNA was demonstrated in extracts of total RNA from the wild-type strain, and also with in vitro synthesized RNAs. Ribonuclease T1 digestion experiments revealed that the ribosome binding site of the hla transcript is blocked by intramolecular base-pairing. Hybridization with RNAIII prevents this intramolecular base-pairing and makes the hla mRNA accessible for translation initiation. This is, to our knowledge, the first example of an 'antisense RNA' that stimulates translation of the target mRNA.[1]References
- Activation of alpha-toxin translation in Staphylococcus aureus by the trans-encoded antisense RNA, RNAIII. Morfeldt, E., Taylor, D., von Gabain, A., Arvidson, S. EMBO J. (1995) [Pubmed]
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