Genetic and Functional Analyses of the mob Operon on Conjugative Transposon, CTn341, from Bacteroides spp.

15:14 EDT 24th May 2015 | BioPortfolio

Summary of "Genetic and Functional Analyses of the mob Operon on Conjugative Transposon, CTn341, from Bacteroides spp."

Bacteroides are Gram-negative anaerobes indigenous to the intestinal tract of humans and they are important opportunistic pathogens. Mobile genetic elements such as conjugative transposons (CTn's) have contributed to an increase in antibiotic resistance in these organisms. CTn's are self-transmissible elements that belong to the superfamily of Integrating Conjugative Elements (ICE's). CTn341 is 52 kb, encodes tetracycline resistance and its transfer is induced by tetracycline. The mobilization region of CTn341 was shown to be comprised of a three gene operon, mobABC, and the transfer origin, oriT. The three genes code for a nicking accessory protein, relaxase and a VirD4-like coupling protein respectively. The Mob proteins were predicted mediate formation of the relaxosome complex, nick DNA at the oriT, and shuttle the DNA/protein complex to the mating pore apparatus. Mutational studies indicated the three genes are required for maximal transfer of CTn341. Mob gene transcription was induced by tetracycline and this regulation was mediated through the two component regulatory system, RteAB. The oriT region of CTn341 was located within 100 bp of mobA and a putative Bacteroides consensus nicking site was observed within this region. Mutation of the putative nick site resulted in a loss of transfer. This study demonstrated a role of the mobilization region for transfer of Bacteroides CTn's and that tetracycline induction occurs for the tra gene operon(s) as shown previously as well as the mob gene operon as reported here.

Affiliation

Department of Microbiology & Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834.

Journal Details

This article was published in the following journal.

Name: Journal of bacteriology
ISSN: 1098-5530
Pages:

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