Beschreibung:
<jats:title>ABSTRACT</jats:title>
<jats:p>
<jats:italic>Mycoplasma gallisepticum</jats:italic>
is a flask-shaped organism that commonly induces chronic respiratory disease in chickens and infectious sinusitis in turkeys. Phenotypic switching in
<jats:italic>M. gallisepticum</jats:italic>
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
<jats:italic>gapA</jats:italic>
gene as part of the same transcription unit. In clones derived from strain R
<jats:sub>low</jats:sub>
, 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
<jats:italic>gapA</jats:italic>
structural gene. In HA
<jats:sup>−</jats:sup>
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
<jats:sup>−</jats:sup>
mutant deficient in producing CrmA, mHAD3, was obtained by disrupting the
<jats:italic>crmA</jats:italic>
gene by using transposition mutagenesis. Despite a fully functional
<jats:italic>gapA</jats:italic>
gene, the amount of GapA detected in this mutant was considerably lower than in HA
<jats:sup>+</jats:sup>
clonal variants, suggesting that, in absence of CrmA, GapA might be subjected to a higher turnover.
</jats:p>