Mycoplasma arthritidis 158L3-1

This genus currently comprizes more than 120 obligate parasitic species found in the wide spectrum of hosts, including humans, animals, insects and plants. Infection that proceeds through attachment of the bacteria to the host cell via specialized surface proteins, adhesins, and subsequent invation, results in prolonged intracellular persistence that may cause lethality. One mechanism by which many mycoplasmas evade the host's adaptive immune responses is through the phase-variable production of critical surface proteins. In some cases, phase variation is achieved by slipped-strand mispairing (SSM) at a run of homonucleotides located upstream of the gene's coding region. Gain or loss of nucleotides in this region acts as an ON/OFF switch for promoter activity by changing the spacing between the promoter's -10 and -35 regions. All mycoplasmas are phenotypically distinguished from other bacteria by their small size (0.3-0.8 micron in diameter) and lack of a cell wall. The latter is one of the major traits that puts them in the separate taxonimic group of microorganisms, class Mollicutes. The cell membrane is rich in protein component (up to two thirds of the membrane mass) that to a great extent consists of highly structurally adaptive lipoproteins employed in invading the host immune system, attachment to the host cells and pathogenic invasion. Most mycoplasmas are non-motile, with the exception of a few flask-shaped human and animal pathogens (M. pneumoniae, M. genitalium, M. gallisepticum, M. pulmonis and M. mobile). Motile mycoplasmas glide over surfaces by an unknown mechanism that is suspected to employ an actin-like cytoskeletal component as well as motility proteins unique for this microbial group. Cell division proceeds via normal binary fission or via elongation of a parent cell to multinucleate filaments and subsequent breakup into coccoid bodies. Mycoplasmas carry the smallest genomes of self-replicating cells (less than 500 recognizable coding regions), which is one of the reasons they were among the first microorganisms selected for the genome-sequencing projects. Examination of the mycoplasmal genomic data indicates the biochemical pathways where gene reductions took place, and helps define the set of genes essential for a minimal self-replicating cell. During their evolution, mycoplasmas appear to have lost all the genes involved in amino acid and cofactor biosynthesis, synthesis of the cell wall and lipid metabolism, resulting in the requirement of the full spectrum of the substrates and factors taken up from the host or from the complex artificial culture medium. The majority of mycoplasmas are deficient in genes coding for components of intermediary and energy metabolism and thus depend mostly on glycolysis as an ATP-denerating pathway. Mycoplasma arthritidis (strain 158L3-1) causes arthritis in both rats and mice. This strain carries a lysogenic bacteriophage, MAV1, integrated into the chromosome. MAV1 supplies important virulence factors to the bacterium. Most mycoplasma rely on the glycolytic pathway for energy production, but several species such as Mycoplasma arthritidis are nonglycolytic and generally catabolize arginine as a major source of energy. The absence of genes in M. arthritidis coding for hexokinase and phosphofuctokinase is consistent with an organism that does not perform glycolysis. (EBI Integr8)