Ribosome Hibernation: Tolerance to Antibiotics

Abstract

In bacteria, ribosomes play an important role in protein synthesis mainly at the translational level. Several environmental factors also contribute to determine the translational activity of a bacterial cell. In adverse conditions such as stress or lack of nutrition the ribosomes reduces its translational activity by a process termed as ribosomal hibernation. It includes the formation of functionally inactive 100S ribosome by the dimerization of two 70S ribosomes [1]. The 100S ribosome formation involves the ribosome modulation factor (RMF) and hibernation promoting factors (HPF). A study conducted by Yoshida and co-workers studied in detail the role of RMF and found that it inactivates the ribosomes by covering the peptidyl transferase centre and entrance of peptide exit tunnel [2]. Similarly, HPF also promotes the dimerization of the ribosomes. A study conducted by Ueta et al. evaluated the process of 100S ribosome formation and pointed out that RMF contributes in 90S immature ribosome genesis and binding of HPF convert this 90S ribosome into mature 100S ribosome [3]. In gram negative and gram positive bacteria the mechanism of dimerization varies. In gram negative bacteria both the factors RMF and HPF play a prominent role in dimerization whereas in gram positive bacteria studies have shown the lack of RMF participation in process of hibernation formation. The presence of single long HPF having the C terminus extension is known to promote the ribosomal dimerization in stressful conditions. A study conducted by Basu and coworkers on dimerization of the ribosomes in Staphylococcus aureus found that the ribosome hibernation promoted the Staphylococcal survival as well as suggested that the disruption of the 100S ribosome may lead to the increase in the efficacy of the conventional antibiotic treatment [4].