Predominant Single Stable VpmaV Expression in Strain GM139 and Major Differences with Mycoplasma agalactiae Type Strain PG2

Abstract

Although mycoplasmas have a reduced genome and no cell wall, they have important mechanisms for the antigenic variation in surface lipoproteins that modulate their interactions with the host. Mycoplasma agalactiae, the main etiological agent of contagious agalactia, has a multigene family involved in the high-frequency phase variation in surface lipoproteins called variable proteins of M. agalactiae (Vpmas). The Vpma lipoproteins are involved in the immune evasion, colonization, dissemination, and persistence of M. agalactiae in the host. In this paper, we evaluate the Vpma phenotypic profiles of two different strains of M. agalactiae, namely, GM139 and the type strain PG2, to assess possible correlations between Vpma phase variability and the geographic localization, animal origin, and pathogenicity of these two strains. Using monospecific Vpma antibodies against individual Vpmas in immunoblots, we demonstrate that, unlike PG2, which expresses six Vpma proteins with high-frequency phase variation, colonies of GM139 predominantly express VpmaV and do not exhibit any sectoring phenotype for any Vpma. Since VpmaV is one of the most important Vpmas for cell adhesion and invasion, its predominant sole expression in GM139 without high-frequency variation may be the basis of the differential pathogenicity of GM139 and PG2. Additionally, MALDI-ToF MS analysis also demonstrates significant differences between these two strains and their relatedness with other M. agalactiae strains.

In silico structural homology modeling and functional characterization of Mycoplasma gallisepticum variable lipoprotein hemagglutin proteins

“…Antigenic variation or phenotypic switching occurs due to high frequency genetic mutations. Due to the lack of a rigid cell wall, the lipoproteins in the mycoplasma cell membrane function as the major elements that come into contact with the host environment ( 45 , 46 , 50 ). These proteins undergo antigenic variation through on/off switching, domain shuffling, and size variation to modify the antigenic components on their cell surface to produce heterotypes that allow mycoplasma to evade recognition and clearance by host immune cells that largely eliminate homo-types.…”