Staphylococcus aureus chromosomal mutation specifically affecting the copy number of Inc3 plasmids

Plasmid ◽  
1983 ◽  
Vol 10 (2) ◽  
pp. 130-137 ◽  
Author(s):  
Serban Iordanescu
Keyword(s):  
Staphylococcus Aureus ◽  
Copy Number ◽  
Chromosomal Mutation

Deletion mutant analysis of the Staphylococcus aureus plasmid pI258 mercury-resistance determinant

1991 ◽  
Vol 37 (8) ◽  
pp. 624-631 ◽  
Author(s):  
Kenneth Babich ◽  
Mike Engle ◽  
Jeffery S. Skinner ◽  
Richard A. Laddaga
Keyword(s):  
Staphylococcus Aureus ◽  
Ion Transport ◽  
Copy Number ◽  
Deletion Mutant ◽  
Resistance Determinant ◽  
Mercury Resistance ◽  
Mutant Analysis ◽  
Mer Operon ◽  
Copy Number Plasmid ◽  
High Copy Number Plasmid

Deletion mutant analysis of the mercury-resistant determinant (mer operon) from the Staphylococcus aureus plasmid pI258 was used to verify the location of the merA and merB genes and to show the existence of mercuric ion transport gene(s). ORF5 was confirmed to be a transport gene and has an amino acid product sequence homologous to the merT gene products from several gram-negative bacteria and a Bacillus species. Deletion analysis established that inactivation of merA on a broad-spectrum mer resistance determinant resulted in a mercury-hypersensitive phenotype. Gene dosage had no apparent effect on the level of resistance conferred by the intact mer operon or on the expression of an inducible phenotype, except that when the intact pI258 mer operon was on a high copy number plasmid, uninduced cells possessed a volatilization rate that was at most only 3.5-fold less than that observed for induced cells. There was no need for mercury ion transport proteins for full resistance when the mer operon was expressed in a high copy number plasmid. Key words: mercury resistance, Staphylococcus aureus plasmid.

scholarly journals Analysis of methicillin-resistant Staphylococcus aureus by IS1181 profiling

1998 ◽  
Vol 120 (3) ◽  
pp. 271-279 ◽  
Author(s):  
C. SYMMS ◽  
B. COOKSON ◽  
J. STANLEY ◽  
J. V. HOOKEY
Keyword(s):  
Staphylococcus Aureus ◽  
Copy Number ◽  
Type Strain ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Phage Type ◽  
Cross Infection ◽  
Insertion Element ◽  
Methicillin Resistant ◽  
Genomic Location ◽  
Strain Nctc

Variation in the genomic location and copy number of the insertion element IS1181 in methicillin-resistant Staphylococcus aureus (MRSA) was investigated. Sixty-three isolates representing the Jevons type strain (NCTC 10442), phage-propagating strains, and epidemic strains were examined. A PCR amplicon of the insertion element was used to probe genomic restriction endonuclease digests. HindIII genomic digests gave 25 distinct IS1181 patterns, while EcoRI digests gave 20 patterns. EMRSA-01, -02, -04, -06, -07, -09, -10, -11, -13 and -14 contained the element but could not be subtyped by profiling it. EMRSA-16 did not contain IS1181, consistent with a unique evolutionary origin for this major UK epidemic strain. Marked heterogeneity was observed among isolates of EMRSA-03. Each EMRSA-03 strain examined gave a unique pattern, thereby allowing subtyping of an important epidemic phage type for the purposes of hospital cross-infection control.

Polymicrobial interactions influence the agr copy number in Staphylococcus aureus isolates from diabetic foot ulcers

2018 ◽  
Vol 111 (11) ◽  
pp. 2225-2232 ◽  
Author(s):  
Carina Matias ◽  
Isa Serrano ◽  
Sofia Van-Harten ◽  
Carla Mottola ◽  
João J. Mendes ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Diabetic Foot ◽  
Copy Number ◽  
Foot Ulcers ◽  
Diabetic Foot Ulcers

Stable low-copy-number Staphylococcus aureus shuttle vectors

Microbiology ◽  
2003 ◽  
Vol 149 (3) ◽  
pp. 785-794 ◽  
Author(s):  
Steve Grkovic ◽  
Melissa H. Brown ◽  
Kate M. Hardie ◽  
Neville Firth ◽  
Ronald A. Skurray
Keyword(s):  
Staphylococcus Aureus ◽  
Copy Number ◽  
Shuttle Vectors ◽  
Low Copy Number

scholarly journals Transcription of the Toxin Genes Present within the Staphylococcal Phage φSa3ms Is Intimately Linked with the Phage's Life Cycle

2003 ◽  
Vol 185 (23) ◽  
pp. 6841-6851 ◽  
Author(s):  
Paul Sumby ◽  
Matthew K. Waldor
Keyword(s):  
Staphylococcus Aureus ◽  
Life Cycle ◽  
Mitomycin C ◽  
Virulence Factors ◽  
Genome Sequence ◽  
Binding Sites ◽  
Copy Number ◽  
Fibrinolytic Enzyme ◽  
Band Shift ◽  
Factors Influencing

ABSTRACT φSa3ms, a lysogenic bacteriophage encoding the staphylococcal enterotoxins SEA, SEG, and SEK and the fibrinolytic enzyme staphylokinase (Sak), was identified in the unannotated genome sequence of the hypervirulent community-acquired Staphylococcus aureus strain 476. We found that mitomycin C induction of φSa3ms led to increased transcription of all four virulence factors. The increase in sea and sak transcription was a result of read-through transcription from upstream latent phage promoters and an increase in phage copy number. The majority of the seg2 and sek2 transcripts were shown to initiate from the upstream phage cI promoter and hence were regulated by factors influencing cI transcription. The lysogeny module of φSa3ms was shown to have some λ-like features with divergent cI and cro genes. Band shift assays were used to identify binding sites for both CI and Cro within the region between these genes, suggesting a mechanism of control for the φSa3ms lytic-lysogenic switch. Our findings suggest that the production of phage-encoded virulence factors in S. aureus may be regulated by processes that govern lysogeny.

scholarly journals rRNA Operon Copy Number Can Explain the Distinct Epidemiology of Hospital-Associated MRSA

2016 ◽  
pp. AAC.01613-16 ◽  
Author(s):  
A.C. Fluit ◽  
M.D Jansen ◽  
T. Bosch ◽  
W.T.M. Jansen ◽  
L. Schouls ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Staphylococcus Aureus ◽  
Copy Number ◽  
Rrna Operon ◽  
Hospital Environment ◽  
Wild Type ◽  
Resistance Development ◽  
Methicillin Resistant ◽  
Resistance Profile

The distinct epidemiology of original hospital-associated methicillin-resistantStaphylococcus aureus(HA-MRSA) and early community-associated MRSA is largely unexplained.S. aureuscarries either 5 or 6 rRNA operon copies. Evidence is provided for a scenario in which MRSA has adapted to the hospital environment by rRNA operon loss (6 to 5 copies) due to antibiotic pressure. Early CA-MRSA in contrast results from wild-type MSSA that acquiredmecAwithout loss of a rRNA operon. Of the HA-MRSA isolates (n=77) 67.5% had five rRNA operon copies compared to 23.2% of the CA-MRSA (n=69) and 7.7% of MSSA isolates (n=195) (p< 0.001). In addition, 105 MSSA isolates of cystic fibrosis patients were tested, because these patients are repeatedly treated with antibiotics and 32.4% of these isolates had five rRNA operon copies. For all subsets a correlation between resistance profile and rRNA copy number was found. Furthermore, we showed thatin vitroantibiotic pressure may result in rRNA operon copy loss. We also showed that without antibiotic pressureS. aureuscontaining six rRNA copies are more fit than isolates with five copies. We conclude that HA-MRSA and cystic fibrosis isolates most likely have been adapted to an environment with high antibiotic pressure by the loss of a rRNA operon copy. This loss has facilitated resistance development, which promoted survival in these niches. However, strain fitness decreased, which explains their lack of success in the community. In contrast, CA-MRSA retained six rRNA operon copies rendering them fitter and thereby able to survive and spread in the community.

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