We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Diversity of silver resistance genes in IncH incompatibility group plasmids.
Microbiology 2001 December
Silver compounds are used as antimicrobial agents in medicine and bacteria that develop resistance to silver cations (Ag(+)) pose problems similar to those of antibiotic-resistant bacteria. The first set of Ag(+) resistance genes (sil) was from plasmid pMG101, now assigned to the IncHI incompatibility group. Questions of whether sil genes are unique to pMG101 or are more widely found, and whether they are associated with a specific incompatibility group or occur in many plasmid groups and on bacterial chromosomes were addressed. sil genes were identified in five IncH plasmids, but not in plasmids of the IncP incompatibility group. Three sil genes (silP, silR and silE) from these plasmids were PCR-amplified, cloned, sequenced and compared to those of pMG101. Differences of 0-50 nt per kb of sequence were found. Predicted gene products were 0-6% different in amino acid sequence, but the differences did not alter residues thought to be involved in protein function (see supplementary data at https://mic.sgmjournals.org or https://www.uic.edu/depts/mcmi/individual/gupta/index.htm). For representative IncH plasmid R476b and pMG101 the effects of Ag(+) exposure on resistance levels were measured by growth. The inducibility of silC, silR and silE gene expression after Ag(+) exposure was studied by reverse transcriptase (RT)-PCR. Silver resistance increased after Ag(+) exposure for strains carrying plasmid R476b. silC and silE expression from R476b was inducible after Ag(+) exposure and was constitutive and high from pMG101. The mRNA levels for the regulatory gene silR was constitutive for both pMG101 and R476b. Close homologues for silABC(ORF96)RS from pMG101 are clustered on the chromosomes of Escherichia coli strains K-12 and O157:H7, without contiguous silP and silE homologues. Insertion deletions of the E. coli K-12 chromosomal homologues for silA and silP gave Ag(+) hypersensitivity for growth. The silA homologue knockout was complemented back to wild-type resistance by the same gene cloned on a plasmid. Homologues of sil genes have also been identified on other enterobacterial genomes.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app