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Mycoplasma gallisepticum , the most pathogenic mycoplasma in poultry, is able to glide over solid surfaces. Although this gliding motility was first observed in 1968, no specific protein has yet been shown to be involved in gliding. We examined  M. gallisepticum  strains and clonal variants for motility and found that the cytadherence proteins GapA and CrmA were required for gliding. Loss of GapA or CrmA resulted in the loss of motility and hemadsorption and led to drastic changes in the characteristic flask-shape of the cells. To identify further genes involved in motility, a transposon mutant library of  M. gallisepticum  was generated and screened for motility-deficient mutants, using a screening assay based on colony morphology. Motility-deficient mutants had transposon insertions in  gapA  and the neighbouring downstream gene  crmA.  In addition, insertions were seen in gene  mgc2,  immediately upstream of  gapA,  in two motility-deficient mutants. In contrast to the GapA/CrmA mutants, the  mgc2  motility mutants still possessed the ability to hemadsorb. Complementation of these mutants with a  mgc2- hexahistidine fusion gene restored the motile phenotype. This is the first report assigning specific  M. gallisepticum  proteins to involvement in gliding motility.   Electronic supplementary material  The online version of this article (doi:10.1186/s13567-014-0099-2) contains supplementary material, which is available to authorized users.

First identification of proteins involved in motility of Mycoplasma gallisepticum