Abstract
Certain monoclonal antibodies and polyclonal antisera directed to pMGA, the major protein of Mycoplasma gallisepticum, were tested for the ability to influence the surface phenotype of the cell population which resulted from their inclusion in growth medium. The polyclonal antiserum and one monoclonal antibody (MAb 66) resulted in an alteration of surface phenotype; specifically, populations of cells grown either on plates or in broth cultures which contained these reagents ceased the expression of pMGA and instead expressed an antigenically unrelated new polypeptide (p82). Upon the removal of antibody, the progeny of these cells regained pMGA expression and produced antigenically sectored colonies. The basis of this switch between pMGA+ and pMGA- states was shown to be transcriptional. The p82 polypeptide, the expression of which resulted from growth of cells in antibodies, was another member of the pMGA gene family and was located just downstream from the pMGA gene normally expressed by the M. gallisepticum cells used. Collectively the results of this work suggest that this organism has evolved an unusual means of altering the antigenic composition of its surface in response to antibodies or to other environmental cues.
MeSH Terms
Amino Acid Sequence
Antibodies, Bacterial/pharmacology
Antibodies, Monoclonal/pharmacology
Antibody Specificity
Bacterial Proteins/biosynthesis,genetics
Gene Expression Regulation, Bacterial
Genes, Bacterial
Genetic Linkage
Membrane Proteins/biosynthesis,genetics
Molecular Sequence Data
Multigene Family
Mycoplasma/drug effects,genetics,immunology
Periodicity
Phenotype
Sequence Homology, Amino Acid
Transcription, Genetic/drug effects
Chemicals
Antibodies, Bacterial
Antibodies, Monoclonal
Bacterial Proteins
M9 protein, Mycoplasma gallisepticum
Membrane Proteins
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Markham P F
Department of Veterinary Science, The University of Melbourne, Parkville, Victoria, Australia 3052.
Glew M D
Browning G F
Whithear K G
Walker I D
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