SB2013 L04gr5: Difference between revisions

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[[Image:Dimerized VlsE.jpg]]
[[Image:Dimerized VlsE.jpg]]
Figure 2 shows the possible dimerization of VlsE.
  Figure 2 shows the possible dimerization of VlsE.
=Antigenic Variation=
=Antigenic Variation=
Antigenic variation is the process through which an organism is able to evade its host’s immune system.  The antigenic variation that occurs in VlsE uses a complex genetic conversion mechanism that is seen to be concentrated in the VRs. The complex genetic system for VlsE is located near the right telomere on a 28-kb linear plasmid (lp28-1) in strains of B. burgdorferi.  This [http://en.wikipedia.org/wiki/Locus_%28genetics%29 locus] has been shown to be a crucial element for the persistence and virulence of Lyme disease (Bankhead and Chaconas 2007).  The vls antigenic variation locus consists of a vls expression site (vlsE) and 15 silent vls cassettes that reside just upstream of the site.  The vlsE cassette region, which is the variable domain and doesn’t include the invariable amino or carboxyl termini, has approximately 92% DNA sequence identity with the silent vls cassettes.  However, the silent vls cassettes lack promoter sequences and are therefore not expressed.  Throughout the course of infection, the sequences for the flanking termini and the silent vls cassettes are conserved while the vlsE sequence is recombined.  This suggests that the genetic variation mechanism occurs by copying segments of the 15 silent vls cassettes and completely replacing corresponding segments of vlsE sequences.  The resulting differences are centralized in the highly variable regions of the vls cassettes.  This allows for the constant evolution of the VR structures and evades the antibodies of the host immune system (Zhang and Norris 1998).
Antigenic variation is the process through which an organism is able to evade its host’s immune system.  The antigenic variation that occurs in VlsE uses a complex genetic conversion mechanism that is seen to be concentrated in the VRs. The complex genetic system for VlsE is located near the right telomere on a 28-kb linear plasmid (lp28-1) in strains of B. burgdorferi.  This [http://en.wikipedia.org/wiki/Locus_%28genetics%29 locus] has been shown to be a crucial element for the persistence and virulence of Lyme disease (Bankhead and Chaconas 2007).  The vls antigenic variation locus consists of a vls expression site (vlsE) and 15 silent vls cassettes that reside just upstream of the site.  The vlsE cassette region, which is the variable domain and doesn’t include the invariable amino or carboxyl termini, has approximately 92% DNA sequence identity with the silent vls cassettes.  However, the silent vls cassettes lack promoter sequences and are therefore not expressed.  Throughout the course of infection, the sequences for the flanking termini and the silent vls cassettes are conserved while the vlsE sequence is recombined.  This suggests that the genetic variation mechanism occurs by copying segments of the 15 silent vls cassettes and completely replacing corresponding segments of vlsE sequences.  The resulting differences are centralized in the highly variable regions of the vls cassettes.  This allows for the constant evolution of the VR structures and evades the antibodies of the host immune system (Zhang and Norris 1998).