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Surface diversity in Mycoplasma agalactiae is driven by site-specific DNA inversions within the vpma multigene locus

Michelle D Glew1, Marc Marenda, Renate Rosengarten

  • 1Institute of Bacteriology, Mycology and Hygiene, University of Veterinary Medicine, 1210 Vienna, Austria.

Journal of Bacteriology
|October 11, 2002
PubMed

Insights

Mycoplasma agalactiae switches variable surface Vpma proteins through site-specific DNA recombination. This process, controlled by the xer1 recombinase, allows the pathogen to evade host immunity during infection.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Mycoplasma agalactiae causes disease in ruminants.
  • Variable surface lipoproteins (Vpmas) are key virulence factors.
  • Vpma switching is linked to DNA rearrangements and pathogenesis.

Purpose of the Study:

  • To characterize the vpma gene locus in M. agalactiae.
  • To investigate the mechanism of vpma DNA rearrangements.
  • To identify the genetic factors responsible for vpma switching.

Main Methods:

  • Characterization of six vpma genes in M. agalactiae PG2.
  • Analysis of vpma loci from consecutive clonal isolates.
  • Homology searches for genes adjacent to the vpma locus.

Main Results:

  • All vpma genes are clustered and share conserved regions.
  • DNA rearrangements are site-specific, occurring within a 21 bp region.
  • A gene, xer1, homologous to lambda integrase family recombinases, is adjacent to the vpma locus.

Conclusions:

  • A site-specific recombination mechanism controls vpma gene expression.
  • The xer1 gene likely encodes a recombinase responsible for vpma switching.
  • This switching mechanism is crucial for M. agalactiae pathogenesis.

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