Figure 6
Proposed model of target inhibition by apidaecin. Apidaecin competitevly binds with release factors (RF) to the A-site of ribosomes, and inhibits the termination step of translation. This accounts for the stop codon-dependent inhibition of translation by apidaecin in vivo (Fig. 4c) and in vitro (Fig. 5a). Overexpression of PrfA (RF1) reduced sensitivity against apidaecin (Fig. 3b), presumably because the binding of apidaecin to ribosome is reversible. This could be the reason for the static antimicrobial effects of apidaecin.
