Plasmid p576 complete sequence
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB27729 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Nucleotide sequence analysis of the plasmid pVWEx1 by Illumina sequencing technology.
| PRJEB20605 | ENA
Project description:Integrative and conjugative elements (ICEs), a.k.a., conjugative transposons, are mobile genetic elements involved in many biological processes, including the spread of antibiotic resistance. Unlike conjugative plasmids that are extra-chromosomal and replicate autonomously, ICEs are integrated in the chromosome and replicate passively during chromosomal replication. It is generally thought that ICEs do not replicate autonomously. We found that when induced, Bacillus subtilis ICEBs1 replicates as a plasmid. The ICEBs1 origin of transfer (oriT) served as the origin of replication and the conjugal DNA relaxase served as the replication initiation protein. Autonomous replication of ICEBs1 conferred genetic stability to the excised element, but was not required for mating. The B. subtilis helicase PcrA that mediates unwinding and replication of Gram-positive rolling circle replicating plasmids was required for ICEBs1 replication and mating. Nicking of oriT by the relaxase and unwinding by PcrA likely directs transfer of a single-strand of ICEBs1 into recipient cells. This SuperSeries is composed of the SubSeries listed below.
2009-10-16 | GSE18380 | GEO
Project description:Chlamydia trachomatis causes chronic inflammatory diseases of the eye and genital tract of global medical importance. The chlamydial plasmid plays an important role in the pathophysiology of these diseases as plasmid-deficient organisms are highly attenuated. The plasmid encodes both noncoding RNAs and eight conserved ORFs of undefined function. To understand plasmid gene function we generated plasmid shuttle vectors with deletions in each of the eight ORFs. The individual deletion mutants were used to transform chlamydiae and the transformants were characterized in terms of plasmid biology and transcriptional profiling. We show that pgp1-2, -6 and -8 are essential for plasmid maintenance while the other ORFs can be deleted and the plasmid stably maintained. We further show that a pgp4 knockout mutant exhibits an in vitro phenotype similar to its isogenic plasmid-less strain in terms of abnormal inclusion morphology and lack of glycogen accumulation. Microarray and qRT-PCR analysis revealed that pgp4 is involved in transcriptional regulation of multiple chromosomal genes; including the glycogen synthase gene glgA. Based on our results, we propose that Pgp1 is a plasmid replicative helicase, Pgp2 is a plasmid replication protein, Pgp4 is a transcriptional regulator of virulence associated chromosomal genes, and Pgp6-8 are plasmid partitioning proteins. These findings have important implications for understanding the plasmid’s role in chlamydial pathogenesis and the development of novel antigenically multivalent live-attenuated chlamydial vaccines.
2013-02-28 | GSE40979 | GEO
Project description:Bacterial defence systems are tightly regulated to avoid autoimmunity. In Type I restriction-modification (R-M) systems, a specific mechanism called restriction alleviation (RA) controls the activity of the restriction module. In the case of the Escherichia coli Type I R-M system EcoKI, RA proceeds through ClpXP-mediated proteolysis of restriction complexes bound to non-methylated sites that appear after replication or reparation of host DNA. Here, we show that RA is also induced in the presence of plasmids carrying EcoKI recognition sites, a phenomenon we refer to as plasmid-induced RA. Further, we show that the anti-restriction behavior of plasmid-borne non-conjugative transposons such as Tn5053, previously attributed to their ardD loci, is due to plasmid-induced RA. Plasmids carrying both EcoKI and Chi sites induce RA in RecA- and RecBCD-dependent manner. However, inactivation of both RecA and RecBCD restores RA, indicating that there exists an alternative, RecA-independent, homologous recombination pathway that is blocked in the presence of RecBCD. Indeed, plasmid-induced RA in a RecBCD-deficient background does not depend on the presence of Chi sites. We propose that processing of random dsDNA breaks in plasmid DNA via homologous recombination generates non-methylated EcoKI sites, which attract EcoKI restriction complexes channeling them for ClpXP-mediated proteolysis.
2024-06-23 | PXD050621 | Pride
Project description:Positive selection inhibits plasmid coinfection
| PRJEB38218 | ENA