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Infection and Immunity, March 2003, p. 1265-1273, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1265-1273.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Phenotypic Switching in Mycoplasma gallisepticum Hemadsorption Is Governed by a High-Frequency, Reversible Point Mutation

Florian Winner,{dagger} Ivana Markovà, Peter Much,{ddagger} Albin Lugmair, Karin Siebert-Gulle, Gunther Vogl, Renate Rosengarten, and Christine Citti*

Institute of Bacteriology, Mycology and Hygiene, University of Veterinary Medicine Vienna, A-1210 Vienna, Austria

Received 4 September 2002/ Returned for modification 23 October 2002/ Accepted 21 December 2002

Mycoplasma gallisepticum is a flask-shaped organism that commonly induces chronic respiratory disease in chickens and infectious sinusitis in turkeys. Phenotypic switching in M. gallisepticum hemadsorption (HA) was found to correlate with phase variation of the GapA cytadhesin concurrently with that of the CrmA protein, which exhibits cytadhesin-related features and is encoded by a gene located downstream of the gapA gene as part of the same transcription unit. In clones derived from strain Rlow, detailed genetic analyses further revealed that on-off switching in GapA expression is governed by a reversible base substitution occurring at the beginning of the gapA structural gene. In HA- variants, this event generates a stop codon that results in the premature termination of GapA translation and consequently affects the expression of CrmA. Sequences flanking the mutation spot do not feature any repeated motifs that could account for error-prone mutation via DNA slippage and the exact mechanism underlying this high-frequency mutational event remains to be elucidated. An HA- mutant deficient in producing CrmA, mHAD3, was obtained by disrupting the crmA gene by using transposition mutagenesis. Despite a fully functional gapA gene, the amount of GapA detected in this mutant was considerably lower than in HA+ clonal variants, suggesting that, in absence of CrmA, GapA might be subjected to a higher turnover.

* Corresponding author. Mailing address: Institute of Bacteriology, Mycology and Hygiene, University of Veterinary Medicine Vienna, Veterinaerplatz 1, A-1210 Vienna, Austria. Phone: 43-1-25077-2101. Fax: 43-1-25077-2190. E-mail: christine.citti{at}vu-wien.ac.at.

Editor: B. B. Finlay

{dagger} Present address: Lambda GmbH, A-4240 Freistadt, Austria.

{ddagger} Present address: Federal Institute for the Control of Infectious Diseases in Animals, A-2340 Moedling, Austria.

Infection and Immunity, March 2003, p. 1265-1273, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1265-1273.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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