Indikova Ivana, Vronka Martin, Szostak Michael P
Department of Pathobiology, Institute of Bacteriology, Mycology and Hygiene, University of Veterinary Medicine Vienna, Veterinaerplatz 1, A-1210, Vienna, Austria.
Vet Res. 2014 Oct 17;45(1):99. doi: 10.1186/s13567-014-0099-2.
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.
鸡毒支原体是禽类中致病性最强的支原体,能够在固体表面滑行。尽管这种滑行运动早在1968年就被首次观察到,但尚未发现有特定蛋白质参与其中。我们检测了鸡毒支原体菌株和克隆变体的运动能力,发现细胞粘附蛋白GapA和CrmA是滑行所必需的。GapA或CrmA的缺失导致运动能力和血细胞吸附能力丧失,并使细胞特有的烧瓶状形态发生剧烈变化。为了鉴定更多参与运动的基因,构建了鸡毒支原体转座子突变体文库,并基于菌落形态的筛选试验筛选运动缺陷型突变体。运动缺陷型突变体在gapA及其相邻的下游基因crmA中存在转座子插入。此外,在两个运动缺陷型突变体中,在gapA上游紧邻的mgc2基因中也发现了插入。与GapA/CrmA突变体不同,mgc2运动突变体仍具有血细胞吸附能力。用mgc2-六组氨酸融合基因对这些突变体进行互补,恢复了运动表型。这是首次报道特定的鸡毒支原体蛋白参与滑行运动。