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  • 1
    Publication Date: 2013-10-12
    Description: Gram-negative bacteria use the type VI secretion system (T6SS) to translocate toxic effector proteins into adjacent cells. The Pseudomonas aeruginosa H1-locus T6SS assembles in response to exogenous T6SS attack by other bacteria. We found that this lethal T6SS counterattack also occurs in response to the mating pair formation (Mpf) system encoded by broad-host-range IncPalpha conjugative plasmid RP4 present in adjacent donor cells. This T6SS response was eliminated by disruption of Mpf structural genes but not components required only for DNA transfer. Because T6SS activity was also strongly induced by membrane-disrupting natural product polymyxin B, we conclude that RP4 induces "donor-directed T6SS attacks" at sites corresponding to Mpf-mediated membrane perturbations in recipient P. aeruginosa cells to potentially block acquisition of parasitic foreign DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034461/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034461/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, Brian T -- Basler, Marek -- Mekalanos, John J -- AI-018045/AI/NIAID NIH HHS/ -- AI-26289/AI/NIAID NIH HHS/ -- R01 AI018045/AI/NIAID NIH HHS/ -- R01 AI026289/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):250-3. doi: 10.1126/science.1243745.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115441" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibiosis ; Bacterial Secretion Systems/drug effects/*physiology ; *Conjugation, Genetic ; DNA, Bacterial/genetics ; Gene Transfer, Horizontal/drug effects/*physiology ; Plasmids/genetics ; Polymyxin B/pharmacology ; Pseudomonas aeruginosa/drug effects/*genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-10-15
    Description: Bacterial chromosomes often carry integrated genetic elements (for example plasmids, transposons, prophages and islands) whose precise function and contribution to the evolutionary fitness of the host bacterium are unknown. The CTXphi prophage, which encodes cholera toxin in Vibrio cholerae, is known to be adjacent to a chromosomally integrated element of unknown function termed the toxin-linked cryptic (TLC). Here we report the characterization of a TLC-related element that corresponds to the genome of a satellite filamentous phage (TLC-Knphi1), which uses the morphogenesis genes of another filamentous phage (fs2phi) to form infectious TLC-Knphi1 phage particles. The TLC-Knphi1 phage genome carries a sequence similar to the dif recombination sequence, which functions in chromosome dimer resolution using XerC and XerD recombinases. The dif sequence is also exploited by lysogenic filamentous phages (for example CTXphi) for chromosomal integration of their genomes. Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology. We found that acquisition and chromosomal integration of the TLC-Knphi1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif(-) filamentation phenotypes. Furthermore, lysogeny of a dif(-) non-toxigenic V. cholerae with TLC-Knphi1 promoted its subsequent toxigenic conversion through integration of CTXphi into the restored dif site. These results reveal a remarkable level of cooperative interactions between multiple filamentous phages in the emergence of the bacterial pathogen that causes cholera.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967718/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hassan, Faizule -- Kamruzzaman, M -- Mekalanos, John J -- Faruque, Shah M -- R01 AI070963/AI/NIAID NIH HHS/ -- R01 AI070963-02/AI/NIAID NIH HHS/ -- R01 AI070963-03/AI/NIAID NIH HHS/ -- R01 GM068851/GM/NIGMS NIH HHS/ -- R01 GM068851-06/GM/NIGMS NIH HHS/ -- R01 GM068851-07/GM/NIGMS NIH HHS/ -- R01-AI070963/AI/NIAID NIH HHS/ -- R01-GM068851/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):982-5. doi: 10.1038/nature09469. Epub 2010 Oct 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20944629" target="_blank"〉PubMed〈/a〉
    Keywords: Attachment Sites, Microbiological/genetics ; Base Sequence ; Cholera/epidemiology/microbiology ; Cholera Toxin/genetics ; Evolution, Molecular ; Genes, Bacterial/genetics ; Genes, Viral/*genetics ; Genome, Bacterial/genetics ; Genome, Viral/genetics ; Helper Viruses/genetics/physiology ; Humans ; Inovirus/*genetics/pathogenicity/*physiology ; Lysogeny/genetics/physiology ; Molecular Sequence Data ; Phenotype ; Plasmids/genetics ; Prophages/genetics/physiology ; Recombination, Genetic/genetics ; Transduction, Genetic ; Vibrio cholerae/classification/*genetics/pathogenicity/*virology ; Virus Integration/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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