scholarly journals Deletion of One Nucleotide within the Homonucleotide Tract Present in the hsdS Gene Alters the DNA Sequence Specificity of Type I Restriction-Modification System NgoAV

2011 ◽  
Vol 193 (23) ◽  
pp. 6750-6759 ◽  
Author(s):  
M. Adamczyk-Poplawska ◽  
M. Lower ◽  
A. Piekarowicz
Keyword(s):  
Dna Sequence ◽  
Type I ◽  
Sequence Specificity ◽  
Modification System ◽  
Dna Sequence Specificity ◽  
Restriction Modification System ◽  
Restriction Modification

scholarly journals Diversification of the restriction–modification system of Streptococcus pyogenes through its acquisition of mobile elements

2020 ◽  
Author(s):  
Atsushi Ota ◽  
Yukiko Nishiuchi ◽  
Noriko Nakanishi ◽  
Yoshio Iijima ◽  
Tomotada Iwamoto ◽  
...  
Keyword(s):  
Streptococcus Pyogenes ◽  
Complete Genome ◽  
Type I ◽  
Sequence Specificity ◽  
Type Ii ◽  
Genome Sequences ◽  
Modification System ◽  
Dna Sequence Specificity ◽  
Restriction Modification System ◽  
Restriction Modification

ABSTRACTRestriction–modification (RM) systems are typically regarded as “primitive immune systems” in bacteria. The roles of methylation in gene regulation, segregation, and mismatch repair are increasingly recognized. To analyze methyltransferase (MTase) diversity in Streptococcus pyogenes, we compared the RM system distribution in eight new complete genome sequences obtained here and in the database-deposited complete genome sequences of 51 strains. The MTase gene distribution showed that type I MTases often change DNA sequence specificity via switching target recognition domains between strains. The type II MTases in the included strains fell into two groups: a prophage-dominant one and a CRISPR-dominant one. Some highly variable type II MTases were found in the prophage region, suggesting that MTases acquired from phage DNA can generate methylome diversity. Additionally, to investigate the possible contribution of DNA methylation to phenotype, we compared the methylomes and transcriptomes from the four most closely related strains, the results of which suggest that phage-derived methylases possibly regulate the methylome, and, hence, regulate expression levels in S. pyogenes. Our findings will benefit further experimental work on the relationship between virulence genes and pathogenicity in S. pyogenes.

scholarly journals Sau1: a Novel Lineage-Specific Type I Restriction-Modification System That Blocks Horizontal Gene Transfer into Staphylococcus aureus and between S. aureus Isolates of Different Lineages

2006 ◽  
Vol 188 (15) ◽  
pp. 5578-5585 ◽  
Author(s):  
Denise E. Waldron ◽  
Jodi A. Lindsay
Keyword(s):  
Staphylococcus Aureus ◽  
Resistance Genes ◽  
Genetic Manipulation ◽  
Type I ◽  
Sequence Specificity ◽  
Modification System ◽  
Major Mechanism ◽  
Restriction Modification System ◽  
Resistance Transfer ◽  
Restriction Modification

ABSTRACT The Sau1 type I restriction-modification system is found on the chromosome of all nine sequenced strains of Staphylococcus aureus and includes a single hsdR (restriction) gene and two copies of hsdM (modification) and hsdS (sequence specificity) genes. The strain S. aureus RN4220 is a vital intermediate for laboratory S. aureus manipulation, as it can accept plasmid DNA from Escherichia coli. We show that it carries a mutation in the sau1hsdR gene and that complementation restored a nontransformable phenotype. Sau1 was also responsible for reduced conjugative transfer from enterococci, a model of vancomycin resistance transfer. This may explain why only four vancomycin-resistant S. aureus strains have been identified despite substantial selective pressure in the clinical setting. Using a multistrain S. aureus microarray, we show that the two copies of sequence specificity genes (sau1hsdS1 and sau1hsdS2) vary substantially between isolates and that the variation corresponds to the 10 dominant S. aureus lineages. Thus, RN4220 complemented with sau1hsdR was resistant to bacteriophage lysis but only if the phage was grown on S. aureus of a different lineage. Similarly, it could be transduced with DNA from its own lineage but not with the phage grown on different S. aureus lineages. Therefore, we propose that Sau1 is the major mechanism for blocking transfer of resistance genes and other mobile genetic elements into S. aureus isolates from other species, as well as for controlling the spread of resistance genes between isolates of different S. aureus lineages. Blocking Sau1 should also allow genetic manipulation of clinical strains of S. aureus.

scholarly journals Complete Genome Sequence of Brevibacterium linens SMQ-1335

2016 ◽  
Vol 4 (6) ◽  
Author(s):  
Alessandra G. de Melo ◽  
Simon J. Labrie ◽  
Jeannot Dumaresq ◽  
Richard J. Roberts ◽  
Denise M. Tremblay ◽  
...  
Keyword(s):  
Complete Genome Sequence ◽  
Open Reading Frames ◽  
Type I ◽  
Industrial Strain ◽  
Modification System ◽  
Brevibacterium Linens ◽  
Restriction Modification System ◽  
New Type ◽  
Restriction Modification ◽  
Reading Frames

Brevibacterium linens is one of the main bacteria found in the smear of surface-ripened cheeses. The genome of the industrial strain SMQ-1335 was sequenced using PacBio. It has 4,209,935 bp, a 62.6% G+C content, 3,848 open reading frames, and 61 structural RNAs. A new type I restriction-modification system was identified.

scholarly journals DNA methylation from a Type I restriction modification system influences gene expression and virulence in Streptococcus pyogenes

2019 ◽  
Vol 15 (6) ◽  
pp. e1007841 ◽  
Author(s):  
Taylor M. Nye ◽  
Kristin M. Jacob ◽  
Elena K. Holley ◽  
Juan M. Nevarez ◽  
Suzanne Dawid ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Streptococcus Pyogenes ◽  
Type I ◽  
Modification System ◽  
Restriction Modification System ◽  
Restriction Modification

scholarly journals Unstable chromosome rearrangements in Staphylococcus aureus cause phenotype switching associated with persistent infections

2019 ◽  
Vol 116 (40) ◽  
pp. 20135-20140 ◽  
Author(s):  
Romain Guérillot ◽  
Xenia Kostoulias ◽  
Liam Donovan ◽  
Lucy Li ◽  
Glen P. Carter ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Genetic Basis ◽  
Host Cells ◽  
Type I ◽  
Modification System ◽  
Persistent Infections ◽  
Restriction Modification System ◽  
Long Read ◽  
Small Colony ◽  
Restriction Modification

Staphylococcus aureus small-colony variants (SCVs) are associated with unusually chronic and persistent infections despite active antibiotic treatment. The molecular basis for this clinically important phenomenon is poorly understood, hampered by the instability of the SCV phenotype. Here we investigated the genetic basis for an unstable S. aureus SCV that arose spontaneously while studying rifampicin resistance. This SCV showed no nucleotide differences across its genome compared with a normal-colony variant (NCV) revertant, yet the SCV presented the hallmarks of S. aureus linked to persistent infection: down-regulation of virulence genes and reduced hemolysis and neutrophil chemotaxis, while exhibiting increased survival in blood and ability to invade host cells. Further genome analysis revealed chromosome structural variation uniquely associated with the SCV. These variations included an asymmetric inversion across half of the S. aureus chromosome via recombination between type I restriction modification system (T1RMS) genes, and the activation of a conserved prophage harboring the immune evasion cluster (IEC). Phenotypic reversion to the wild-type–like NCV state correlated with reversal of the chromosomal inversion (CI) and with prophage stabilization. Further analysis of 29 complete S. aureus genomes showed strong signatures of recombination between hsdMS genes, suggesting that analogous CI has repeatedly occurred during S. aureus evolution. Using qPCR and long-read amplicon deep sequencing, we detected subpopulations with T1RMS rearrangements causing CIs and prophage activation across major S. aureus lineages. Here, we have discovered a previously unrecognized and widespread mechanism of reversible genomic instability in S. aureus associated with SCV generation and persistent infections.

scholarly journals The EcoKI Type I Restriction-Modification System in Escherichia coli Affects but Is Not an Absolute Barrier for Conjugation

2014 ◽  
Vol 197 (2) ◽  
pp. 337-342 ◽  
Author(s):  
Louise Roer ◽  
Frank M. Aarestrup ◽  
Henrik Hasman
Keyword(s):  
Escherichia Coli ◽  
Rapid Evolution ◽  
Type I ◽  
Modification System ◽  
Major Barrier ◽  
Exogenous Dna ◽  
Content Type ◽  
Restriction Modification System ◽  
K 12 ◽  
Restriction Modification

The rapid evolution of bacteria is crucial to their survival and is caused by exchange, transfer, and uptake of DNA, among other things. Conjugation is one of the main mechanisms by which bacteria share their DNA, and it is thought to be controlled by varied bacterial immune systems. Contradictory results about restriction-modification systems based on phenotypic studies have been presented as reasons for a barrier to conjugation with and other means of uptake of exogenous DNA. In this study, we show that inactivation of the R.EcoKI restriction enzyme in strainEscherichia coliK-12 strain MG1655 increases the conjugational transfer of plasmid pOLA52, which carriers two EcoKI recognition sites. Interestingly, the results were not absolute, and uptake of unmethylated pOLA52 was still observed in the wild-type strain (with an intacthsdRgene) but at a reduction of 85% compared to the uptake of the mutant recipient with a disruptedhsdRgene. This leads to the conclusion that EcoKI restriction-modification affects the uptake of DNA by conjugation but is not a major barrier to plasmid transfer.

scholarly journals Plasmid R16 ArdA Protein Preferentially Targets Restriction Activity of the Type I Restriction-Modification System EcoKI

2003 ◽  
Vol 185 (6) ◽  
pp. 2022-2025 ◽  
Author(s):  
Angela T. Thomas ◽  
William J. Brammar ◽  
Brian M. Wilkins
Keyword(s):  
Type I ◽  
Bacterial Conjugation ◽  
Modification System ◽  
Restriction Modification System ◽  
Modification Activity ◽  
Restriction Modification

ABSTRACT The ArdA antirestriction protein of the IncB plasmid R16 selectively inhibited the restriction activity of EcoKI, leaving significant levels of modification activity under conditions in which restriction was almost completely prevented. The results are consistent with the hypothesis that ArdA functions in bacterial conjugation to allow an unmodified plasmid to evade restriction in the recipient bacterium and yet acquire cognate modification.

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