A region containing the blaSHV-5 gene is flanked by two IS26 copies

and its copy number multiplies spontaneously within p1658/97 and RecA-deficient E. coli strains. Here, we demonstrate that the amplified IS26-blaSHV-5 units were arranged in tandems, containing up to more than 10 units, which could raise ceftazidime MICs for host strains from 4 μg mL−1 to more than 128 μg mL−1. Successive deletions within p1658/97, located outside the amplifiable module and encompassing even as little as c. 15% of the plasmid, click here blocked the amplification. Moreover, the complementing re-introduction of the deleted fragments in trans did not restore the process. Similarly, insertions of a 1-kb DNA fragment into the amplicon inhibited its self-multiplication ability. The module was able to transmit into another IS26-containing plasmid by recombination. The results prompted us to speculate that local DNA structure, especially favorable in p1658/97, might have been responsible for the IS26-blaSHV-5 multiplication ability. “
“The Streptococcus mutansComX-regulon encompasses > 200 mostly uncharacterized AZD8055 order genes, including

cinA. Here we report that cinA is regulated by ComX in the presence of the competence stimulating peptide (CSP), wherein loss of CinA (strain SmuCinA) results in reduced transformability with or without added CSP by 74- and 15-fold, respectively (P < 0.003). In CSP-supplemented cultures, a two-fold increase in cell viability was noted for SmuCinA relative to UA159 (P < 0.002), suggesting

CinA’s involvement in the CSP-modulated cell killing response. Relative to UA159, loss of CinA also rendered the mutant hypersensitive to killing by methyl methanesulfonate (MMS), which impairs homologous recombination. Despite our use of a non-polar mutagenesis strategy to knockout cinA, which is the first gene of the multicistronic operon harboring cinA, we noted a drastic reduction in recA expression. By using a Fossariinae CinA-complemented mutant, we were able to partially, but not completely restore all phenotypes to UA159 levels. Complementation results suggested that although cinA participates in modulating competence, viability and MMS tolerance, genes downstream of the cinA transcript may also regulate these phenotypes, a finding that warrants further examination. This is the first report that describes a role for S. mutans’ CinA in contending with DNA damage, genetic transformation and cell survival. Genetic competence is a transient physiological state that facilitates horizontal gene transfer that enables recipient bacteria to acquire novel genes by the uptake of exogenous DNA from the environment (Claverys & Martin, 1998).