Genome Annotation of Five Mycoplasma canis Strains

Brown, Daniel R.; May, Meghan; Michaels, Dina L.; Barbet, Anthony F.

doi:10.1128/jb.00664-12

Cited by 7 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…(Roy and Mukherjee, 2009;Woolery et al, 2010) or from intracellular bacteria directly into the host cell cytoplasm (Shin and Roy, 2008). For example, the alkalescens and M. canis (Brown et al, 2012;Manso-Silván et al, 2013). Although a role in effecting mycoplasmal virulence remains to be established, their absence from a broader spectrum of mycoplasma species argues against a general function in endogenous metabolic regulation by mycoplasmal AMPylators.…”

Section: Candidate Effectorsmentioning

confidence: 99%

“…For the avian pathogen M. gallisepticum the preferred receptors are α-2,6-linked sialo-conjugates [Glasgow and Hill, 1980], and its sialidase, a true homolog of that expressed by M. synoviae (May and Brown, 2009), degrades α-2,6-linkages more efficiently than α-2,3-linked substrates (Sethi and Müller, 1972). Disruption of the sialidase gene in M. gallisepticum resulted in an attenuated phenotype as measured by bacterial recovery rates, tracheal lesion scores, and tracheal thickness measurements in experimentally infected Leghorn chickens, although virulence could not be completely restored by genetic complementation of sialidase activity (May et al, 2012).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Virulence Effectors of Pathogenic Mycoplasmas

May¹,

Brown²

2018

Preprint

View full text Add to dashboard Cite

Members of the genus Mycoplasma and related organisms impose a substantial burden of infectious diseases on humans and animals, but the last comprehensive review of mycoplasmal pathogenicity was published 20 years ago. Post-genomic analyses have now begun to support the discovery and detailed molecular biological characterization of a number of specific mycoplasmal virulence factors. This review covers three categories of defined mycoplasmal virulence effectors: 1) specific macromolecules including the superantigen MAM, the ADP-ribosylating CARDS toxin, sialidase, cytotoxic nucleases, cell-activating diacylated lipopeptides, and phosphocholine-containing glycoglycerolipids; 2) the small molecule effectors hydrogen peroxide, hydrogen sulfide, and ammonia; and 3) several putative mycoplasmal orthologs of virulence effectors documented in other bacteria.  Understanding such effectors and their mechanisms of action at the molecular level connects the biology of the bacteria to direct effects on the host and host responses they elicit, and is expected to translate into new interventions for human and veterinary mycoplasmosis.

show abstract

Section: Candidate Effectorsmentioning

confidence: 99%

mentioning

confidence: 99%

Virulence Effectors of Pathogenic Mycoplasmas

May¹,

Brown²

2018

Preprint

View full text Add to dashboard Cite

show abstract

“…Moreover, nucleotide usage bias and translational selection in prokaryotic genome were considered to be the most important factors in the synonymous codon usage bias and usage bias of nucleotide surrounding a genetic code . Turning to the current studies for nucleotide, synonymous codon, and amino acid usages in mycoplasma genome, there is no report for mycoplasma species, even though there are more and more sequencing genome reports . In this study, the comprehensive analyses of nucleotide, synonymous codon, and amino acid usage patterns for identifying various selection pressures have been done at the whole genomic level by multivariate statistical methods.…”

Section: Introductionmentioning

confidence: 99%

Comparative genomic analysis for nucleotide, codon, and amino acid usage patterns of mycoplasmas

Cao

et al. 2018

J Basic Microbiol

View full text Add to dashboard Cite

The evolutionary factors in influencing the genetic characteristics of nucleotide, synonymous codon, and amino acid usage of 18 mycoplasma species were analyzed. The nucleotide usage at the 1st and 2nd codon position which determines amino acid composition of proteins has a significant correlation with the total nucleotide composition of gene population of these mycoplasma species, however, the nucleotide usage at the 3rd codon position which affects synonymous codon usage patterns has a slight correlation with either the total nucleotide composition or the nucleotide usage at the 1st and 2nd codon position. Other evolutionary factors join in the evolutionary process of mycoplasma apart from mutation pressure caused by nucleotide usage constraint based on the relationships between effective number of codons/codon adaptation index and nucleotide usage at the 3rd codon position. Although nucleotide usage of gene population in mycoplasma dominates in forming the overall codon usage trends, the relative abundance of codon with nucleotide context and amino acid usage pattern show that translation selection involved in translation accuracy and efficiency play an important role in synonymous codon usage patterns. In addition, synonymous codon usage patterns of gene population have a bigger power to represent genetic diversity among different species than amino acid usage. These results suggest that although the mycoplasmas reduce its genome size during the evolutionary process and shape the form, which is opposite to their hosts, of AT usages at high levels, this kind organism still depends on nucleotide usage at the 1st and 2nd codon positions to control syntheses of the requested proteins for surviving in their hosts and nucleotide usage at the 3rd codon position to develop genetic diversity of different mycoplasma species. This systemic analysis with 18 mycoplasma species may provide useful clues for further in vivo genetic studies on the related species.

show abstract

“…Annotation was accomplished via the NCBI Prokaryotic Genome Annotation Pipeline (28). Nucleotide and amino acid sequence similarities to the genomes of previously sequenced strains PG14 T , UF31, UF33, UFG1, and UFG4 (29) were calculated by using JSpecies version 1.2.1 (30) and AAI Calculator (http://enve-omics.ce .gatech.edu/aai).…”

mentioning

confidence: 99%

Cellular Microbiology of Mycoplasma canis

et al. 2016

View full text Add to dashboard Cite

M ycoplasma canis infects many mammalian hosts but is usually thought of as a commensal or opportunistic cofactor in respiratory or urogenital tract diseases of dogs (1). We found unexpectedly that M. canis was also detectable by culture or PCR in a majority of brain tissue specimens in a retrospective case-control study of canine granulomatous meningoencephalitis (ME) (GME) and necrotizing ME (NME) (2). The presence of M. canis in brain tissue was associated with both GME and NME (both P Ͻ 0.05, as determined by a 2 test). The clinical signs of this common idiopathic neurological disease of dogs include seizures, proprioceptive deficits, circling, and blindness. Immunosuppressive therapy may be palliative, but the syndrome is progressive and uniformly fatal (3). The extensive search for a presumed viral cause of canine GME and NME has been fruitless (4).In humans, bacterial meningitis and encephalitis are multifactorial lethal infections with often severe sequelae for survivors. New detection methods have shown that the variety of bacteria associated with human ME is much more extensive than usually appreciated (5-9). Additional animal models of bacterial ME are necessary to study this broader spectrum of pathogens (10). Since a possible association between M. canis and canine ME was discovered, our objective has been to help fill the void of basic knowledge about the organism's virulence factors, the host responses that it elicits, and its potential roles in pathogenesis. Our working hypotheses were that M. canis is capable of evoking host cell responses that favor dissemination from mucosal surfaces to secondary sites of infection, possibly in a strain-dependent fashion, and also that, regardless of how it might reach those sites, the presence of M. canis there modulates inflammation and direct injury to host cells. Understanding this potential can be expected to help evaluate the cause of canine ME and other diseases.(Portions of these data were presented in abstract form at Congresses of the International Organization for Mycoplasmology [90,91].) MATERIALS AND METHODSMycoplasma strains and cultivation. Strain PG14 T of M. canis (ATCC 19525) was first isolated from the throat of a normal dog (11). Strains UF31, UF33, LV, 5, 26, Cal, and Mara were first isolated from vaginal swabs of dogs without ME (12). Strains UFG1, UFG2, UFG3, and UFG4 were isolated from frozen brain tissues from cases of canine NME (2). Mycoplasma cynos strain H-831 T (ATCC 27544) was first isolated from the lung of a dog with pneumonia (13). Mycoplasma arginini strain G230 T , Mycoplasma bovigenitalium strain PG11 T , Mycoplasma edwardii strain PG24 T , Mycoplasma maculosum strain Skotti B, Mycoplasma molare strain H542 T , Mycoplasma opalescens strain MH5408 T , and Mycoplasma spumans strain PG13T , representing other species that have been isolated from dogs (1), were obtained from The Mollicutes Collection. All strains were propagated under standard conditions (14) in ATCC 988 medium supplemented with fetal bovine serum (FBS) and glu...

show abstract

Genome Annotation of Five Mycoplasma canis Strains

Cited by 7 publications

References 11 publications

Virulence Effectors of Pathogenic Mycoplasmas

Virulence Effectors of Pathogenic Mycoplasmas

Comparative genomic analysis for nucleotide, codon, and amino acid usage patterns of mycoplasmas

Cellular Microbiology of Mycoplasma canis

Contact Info

Product

Resources

About