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Infection and Immunity, October 2000, p. 6027-6033, Vol. 68, No. 10
Department of Veterinary Science, The
University of Melbourne, Parkville, Victoria, Australia 3052
Received 9 December 1999/Returned for modification 16 March
2000/Accepted 5 June 2000
Chickens were infected with a pathogenic strain of Mycoplasma
gallisepticum, and the expression of pMGA, the major surface protein, was inferred by examination of colonies from ex vivo cells.
Within 2 days postinfection, 40% of cells had ceased the expression of
the original pMGA surface protein (pMGA1.1), and by day 6, the majority
of recovered cells were in this category. The switch in pMGA phenotype
which had occurred in vivo was reversible, since most colonies produced
from ex vivo progenitors exhibited frequent pMGA1.1+
sectors. After prolonged in vivo habitation, increasing proportions of
recovered cells gave rise to variant pMGA colonies which had switched
from the expression of pMGA1.1 to another gene, pMGA1.2, concomitant
with the acquisition of a (GAA)12 motif 5' to its promoter.
Collectively, the results suggest that changes in M. gallisepticum pMGA gene expression in vivo are normal, common, and possibly obligate events for successful colonization of the host.
Surprisingly, the initial cessation of pMGA1.1 expression occurred in
the absence of detectable pMGA antibodies and seemed to precede
the adaptive immune response.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
pMGA Phenotypic Variation in Mycoplasma gallisepticum
Occurs In Vivo and Is Mediated by Trinucleotide Repeat
Length Variation

*
Corresponding author. Mailing address: Department of
Veterinary Science, The University of Melbourne, Parkville, Victoria, Australia 3052. Phone: 61 3 8344 7352. Fax: 61 3 8344 7374. E-mail: i.walker{at}vet.unimelb.edu.au.
Present address: Institute of Bacteriology and Animal Hygiene,
Vienna University of Veterinary Science, A-1210, Vienna, Austria.
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