BacA-mediated bleomycin sensitivity in Sinorhizobium meliloti is independent of the unusual lipid A modification.
Sinorhizobium meliloti bacA mutants are symbiotically defective, deoxycholate sensitive, and bleomycin resistant. We show that the bleomycin resistance phenotype is independent of the lipid A alteration and that the changes giving rise to both phenotypes are likely to be involved in the inability of bacA mutants to persist within their hosts.
Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. G.Ferguson@ed.ac.uk
Gail P
GP
Ferguson
An
A
Jansen
Victoria L
VL
Marlow
Graham C
GC
Walker
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins / Q000378:metabolism*; D001761:Bleomycin / Q000494:pharmacology*; D003840:Deoxycholic Acid / Q000494:pharmacology; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D017353:Gene Deletion; D005798:Genes, Bacterial; D008050:Lipid A / Q000378:metabolism*; D016962:Sinorhizobium meliloti / Q000187:drug effects* / Q000254:growth & development; D013559:Symbiosis / Q000235:genetics / Q000502:physiology
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D008050:Lipid A; D003840:Deoxycholic Acid; D001761:Bleomycin