The Gene and Putative Peptidase Genes May Be Required for Virulence in Mycoplasma gallisepticum.

Relatively few virulence genes have been identified in pathogenic mycoplasmas, so we used signature-tagged mutagenesis to identify mutants of the avian pathogen with a reduced capacity to persist and compared the levels of virulence of selected mutants in experimentally infected chickens. Four mutants had insertions in one of the two incomplete operons, and a further three had insertions in distinct hypothetical genes, two containing peptidase motifs and one containing a member of a gene family. The three hypothetical gene mutants and the two with insertions in were used to infect chickens, and all five were shown to have a reduced capacity to induce respiratory tract lesions. One mutant and the MGA_1102 and MGA_1079 mutants had a greatly reduced capacity to persist in the respiratory tract and to induce systemic antibody responses against The other mutant and the MGA_0588 mutant had less capacity than the wild type to persist in the respiratory tract but did elicit systemic antibody responses. Although carries two incomplete operons, one of which has been acquired by horizontal gene transfer, our results suggest that one of the copies of may be required for full expression of virulence. We have also shown that three hypothetical genes, two of which encode putative peptidases, may be required for full expression of virulence in None of these genes has previously been shown to influence virulence in pathogenic mycoplasmas.