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- W124833181 abstract "The evolution and emergence of pathogenic bacteria is tightly linked to the horizontal transfer of pathogenicity islands (PAIs) and bacteriophages encoding a range of virulence factors. We studied the evolutionary relationships between integrases and excisionases from a group of islands, and used VPI-2 as a model for pathogenicity island excision. We determined the functional role of the VPI-2-encoded integrase (intVPI-2) and two putative excisionases (vefA and vefB) in excision. We found negligible levels of excision as measured by attB levels in the ΔintVPI-2 strain whereas overexpression of intVPI-2showed an increase in excision. In the ΔvefA excision is severely decreased. Overexpression of vefA (VC1785) in the wildtype causes complete excision of the island, while complimenting vefA in either of the deleted strains ΔvefA and ΔvefB leads to only a minor increase in excision. Overexpression of vefA also causes excision of a second island, VPI, critical for pathogenicity. For the first time, we have demonstrated that a factor encoded on one island, vefA, causes the excision of a second. This work was funded by a NSF career grant to EFB and a Beckman Scholars grant to MGN." @default.
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- W124833181 date "2010-04-01" @default.
- W124833181 modified "2023-09-27" @default.
- W124833181 title "An Evolutionary and Functional Analysis of Vibrio Pathogenicity Island 2" @default.
- W124833181 doi "https://doi.org/10.1096/fasebj.24.1_supplement.877.1" @default.
- W124833181 hasPublicationYear "2010" @default.
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