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P Pilus Assembly Motif Necessary for Activation of the CpxRA Pathway by PapE in Escherichia coli. Yvonne M. Lee, 2004.P pilus biogenesis occurs via the highly conserved chaperone-usher pathway, and assembly is monitored by the CpxRA two-component signal transduction pathway . Structural pilus subunits consist of an N-terminal extension followed by an incomplete immunoglobulin-like fold that is missing a C-terminal seventh beta strand . In the pilus fiber, the immunoglobulin-like fold of each pilin is completed by the N-terminal extension of its neighbor . Subunits that do not get incorporated into the pilus fiber are driven "OFF-pathway." In this study, we found that PapE was the only OFF-pathway nonadhesin P pilus subunit capable of activating Cpx . Manipulation of the PapE structure by removing, relocating within the protein, or swapping its N-terminal extension with that of other subunits altered the protein's self-associative and Cpx-activating properties . The self-association properties of the new subunits were dictated by the specific N-terminal extension provided and were consistent with the order of the subunits in the pilus fiber . However, these aggregation properties did not directly correlate with Cpx induction . Cpx activation instead correlated with the presence or absence of an N-terminal extension in the PapE pilin structure . Removal of the N-terminal extension of PapE was sufficient to abolish Cpx activation . Replacement of an N-terminal extension at either the amino or carboxyl terminus restored Cpx induction . Thus, the data presented in this study argue that PapE has features inherent in its structure or during its folding that act as specific inducers of Cpx signal transduction . Variant Salmonella Genomic Island 1 Antibiotic Resistance Gene Cluster Containing a Novel 3'-N-Aminoglycoside Acetyltransferase Gene Cassette, aac(3)-Id, in Salmonella enterica Serovar Newport. Benoît Doublet, 2004.Salmonella genomic island 1 (SGI1) harbors an antibiotic resistance gene cluster and was previously identified in the multidrug-resistant Salmonella enterica serovars Typhimurium DT104, Agona, Paratyphi B, and Albany . This antibiotic resistance gene cluster is a complex class 1 integron and most often confers resistance to ampicillin (Ap), chloramphenicol (Cm)/florfenicol (Ff), streptomycin (Sm)/spectinomycin (Sp), sulfonamides (Su), and tetracycline (Tc) (ApCmFfSmSpSuTc profile) . Recently, variant SGI1 antibiotic resistance gene clusters conferring different antibiotic resistance profiles have been identified in several S . enterica serovars and were classified as SGI1-A to -G . We identified a new variant SGI1 antibiotic resistance gene cluster in two multidrug-resistant S . enterica serovar Newport strains isolated from humans in France . In these strains, the Sm/Sp resistance gene cassette aadA2 inserted at the first attI1 site was replaced by two other aminoglycoside resistance gene cassettes . The first one contains a new resistance gene encoding an AAC(3)-I aminoglycoside 3-N-acetyltransferase that confers resistance to gentamicin (Gm) and sisomicin (Sc) . This gene has been named aac(3)-Id . The second one harbors the Sm/Sp resistance gene aadA7 . This gene cassette replacement in the SGI1 complex integron of serovar Newport strains constitutes a new variant SGI1 antibiotic resistance gene cluster named SGI1-H . The occurrence of SGI1 in different S . enterica serovars, now including serovar Newport, strengthens the hypothesis of horizontal transfer of SGI1 .
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