Differential metabolism of Mycoplasma species as revealed by their genomes

Abstract

The annotation and comparative analyses of the genomes of Mycoplasma synoviae and Mycoplasma hyopneumonie, as well as of other Mollicutes (a group of bacteria devoid of a rigid cell wall), has set the grounds for a global understanding of their metabolism and infection mechanisms. According to the annotation data, M. synoviae and M. hyopneumoniae are able to perform glycolytic metabolism, but do not possess the enzymatic machinery for citrate and glyoxylate cycles, gluconeogenesis and the pentose phosphate pathway. Both can synthesize ATP by lactic fermentation, but only M. synoviae can convert acetaldehyde to acetate. Also, our genome analysis revealed that M. synoviae and M. hyopneumoniae are not expected to synthesize polysaccharides, but they can take up a variety of carbohydrates via the phosphoenolpyruvate-dependent phosphotransferase system (PEP-PTS). Our data showed that these two organisms are unable to synthesize purine and pyrimidine de novo, since they only possess the sequences which encode salvage pathway enzymes. Comparative analyses of M. synoviae and M. hyopneumoniae with other Mollicutes have revealed differential genes in the former two genomes coding for enzymes that participate in carbohydrate, amino acid and nucleotide metabolism and host-pathogen interaction. The identification of these metabolic pathways will provide a better understanding of the biology and pathogenicity of these organisms

Repetitive Elements in Mycoplasma hyopneumoniae Transcriptional Regulation

“…hyopneumoniae strain 7448 in MHP7448_0087, glyA and sipS genes (Table 3), suggesting that some DNA repeats analysed may be involved in mycoplasma pathogenicity. GTP-binding protein, glycine hydroxymethyltransferase enzyme and signal peptidase I coding genes are important to cell viability and in some cases have already been related to mycoplasma pathogenicity process [55–57]. Promoter sequences associated with tandem repeats were present in all regulatory sequences of experimentally tested genes (S2 Table), reinforcing the hypothesis that repetitive elements may be interfering in the promoter region and consequently the transcription of related genes [20, 54].…”

Interactions of Mycoplasma hyopneumoniae with extracellular traps

“…The differing biochemical activities among Mycoplasma species are vast, but they are united by deficiencies in metabolic capabilities. Mycoplasma species lack pathways for cell wall production, de novo synthesis of purines and pyrimidines, and have truncated respiratory systems to name a few (2,12). Probably the most notable requirement of Mycoplasma species is the need for fatty acids and lipids for membrane synthesis (13,16).…”

“…Through reductive evolution, the genome of M. hyopneumoniae is quite minimal, lacking main biosynthetic pathways such as purine and pyrimidine synthesis (2). Chronic EP can partially be attributed to the loss of cilia along the tracheal epithelium resulting in a nonfunctional mucociliary elevator and the introduction of secondary pathogens (3).…”

“…Mycoplasmas are prokaryotes characterized by the lack of a cell wall (10), contain relatively small genomes (11,12) and belong to the class Mollicutes, Analysis of the 16S ribosomal RNA reveals that Mollicutes likely arose through reductive evolution from the Firmicutes with a gram-positive cell wall and low G+C content (2,11,13). Mycoplasma species have been described to inhabit a variety of hosts worldwide including vertebrate animals, insects, and plants (11,14) and tend to be host specific (14).…”

“…Mycoplasma species have been described to inhabit a variety of hosts worldwide including vertebrate animals, insects, and plants (11,14) and tend to be host specific (14). The small and consequentially minimal genomes of mycoplasmas make these prokaryotes obligate parasites of their hosts; infection tends to be chronic with high morbidity but low mortality (2,11). As is the pattern for most pathogenic bacteria that cause chronic infections of animals, bacteria must prevail through two critical stages of infection.…”