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Antimicrob. Agents Chemother. doi:10.1128/AAC.00870-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Erythromycin- and chloramphenicol-induced ribosomal assembly defects are secondary effects of protein synthesis inhibition

Institute of Molecular and Cell Biology, University of Tartu, Riia 23, Tartu, Estonia; Institute of Technology, University of Tartu, Nooruse 1, Tartu, Estonia; Center for Pharmaceutical Biotechnology, University of Illinois at Chicago, 900 S. Ashland Ave., Chicago, IL 60607, USA

^* To whom correspondence should be addressed. Email: Tanel.Tenson{at}ut.ee.

	Abstract

Several protein synthesis inhibitors are known to inhibit ribosome assembly. This may be a consequence of direct binding of the antibiotic to ribosome precursor particles, or it could result indirectly from loss of coordination in the production of ribosomal components due to the inhibition of protein synthesis. Here we demonstrate that inhibitors of the large ribosomal subunit, erythromycin and chloramphenicol, affect assembly of both the large and small subunits. Expression of a small erythromycin resistance peptide acting in cis on mature ribosomes relieves the erythromycin-mediated assembly defect for both subunits. Erythromycin treatment of bacteria expressing a mixture of erythromycin-sensitive and -resistant ribosomes produced comparable effects on subunit assembly. These results argue in favour of the view that erythromycin and chloramphenicol affect assembly of the large ribosomal subunit indirectly.