This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Gabriel, S. E.
Right arrow Articles by Helmann, J. D.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gabriel, S. E.
Right arrow Articles by Helmann, J. D.

 Previous Article  |  Next Article 

Journal of Bacteriology, October 2009, p. 6116-6122, Vol. 191, No. 19
0021-9193/09/$08.00+0     doi:10.1128/JB.00802-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Contributions of Zur-Controlled Ribosomal Proteins to Growth under Zinc Starvation Conditions{triangledown}

Scott E. Gabriel and John D. Helmann*

Department of Microbiology, Cornell University, Ithaca, New York 14853-8101

Received 19 June 2009/ Accepted 23 July 2009

Maintaining intracellular zinc levels is critical, because zinc serves as a cofactor for many required enzymes and is toxic in excess. Bacillus subtilis Zur, a Fur family repressor, controls the zinc starvation response including two ribosomal proteins (r-proteins) paralogous to L31 and S14. Biochemical analyses suggest that Zur-controlled r-proteins (which lack the two CXXC metal-binding motifs) may functionally replace their cognate zinc-requiring proteins during zinc limitation. We demonstrate here that Zur regulates the expression of an additional r-protein paralog, RpmGC (L33c), and, using strains defective in zinc uptake, we investigate the physiological contributions of all three Zur-regulated r-proteins. In the 168 lineage, rpmGC is a pseudogene containing a frameshift mutation. Correction of this mutation allows expression of a functional L33c that can suppress the poor growth phenotype of an rpmGA rpmGB (encoding L33a, L33b) double mutant. Similarly, we provide physiological evidence in support of the "failsafe" model (Y. Natori et al., Mol. Microbiol. 63:294-307, 2007) in which the Zur-regulated S14 paralog YhzA allows continued ribosome synthesis when there is insufficient zinc to support S14 function. The L31 paralog YtiA can replace L31 and complement the growth defect of an rpmE mutant (Nanamiya et al., Mol. Microbiol. 52:273-283). We show that, under zinc starvation conditions, derepression of YtiA significantly increases the growth of cells in which preexisting ribosomes carry, as the sole L31 protein, RpmE (containing zinc), but not if they carry YtiA (which lacks zinc). These results support a direct and physiologically relevant role for YtiA in mobilizing zinc from ribosomes.

* Corresponding author. Mailing address: Department of Microbiology, Wing Hall, Cornell University, Ithaca, NY 14853-8101. Phone: (607) 255-6570. Fax: (607) 255-3904. E-mail: jdh9{at}cornell.edu

{triangledown} Published ahead of print on 31 July 2009.

Journal of Bacteriology, October 2009, p. 6116-6122, Vol. 191, No. 19
0021-9193/09/$08.00+0     doi:10.1128/JB.00802-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»