ABSTRACT When bacterial lineages make the transition from free-living or facultatively parasitic life cycles to permanent associations with hosts, they undergo a major loss of genes and DNA. Complete genome sequences are providing an understanding of how extreme genome reduction affects evolutionary directions and metabolic capabilities of obligate pathogens and symbionts.
- SourceAvailable from: Christian Kost
[Show abstract] [Hide abstract]
- "The latter scenario likely explains why amino acid biosynthesis pathways are sometimes partitioned between a eukaryotic host and its prokaryotic endosymbiont (Shigenobu et al. 2000) or between multiple co-symbionts (McCutcheon and Moran 2007). A second factor that could explain the loss of genetic information from bacterial genomes is genetic drift (Andersson and Kurland 1998; Moran 2002; Kuo et al. 2009). When bacteria transition from a free-living to a symbiotic lifestyle such as the bacterial endosymbionts of insects (Ochman and Moran 2001; Moran and Plague 2004; McCutcheon and Moran 2007), repeated bottlenecks of relatively small populations may result in a weakened selection even for required genes, thus resulting in an elimination of dispensable genes (Moran et al. 2008). "
ABSTRACT: Bacteria that have adapted to nutrient-rich, stable environments are typically characterized by reduced genomes. The loss of biosynthetic genes frequently renders these lineages auxotroph, hinging their survival on an environmental uptake of certain metabolites. The evolutionary forces that drive this genome degradation, however, remain elusive. Our analysis of 949 metabolic networks revealed auxotrophies are likely highly prevalent in both symbiotic and free-living bacteria. To unravel whether selective advantages can account for the rampant loss of anabolic genes, we systematically determined the fitness consequences that result from deleting conditionally essential biosynthetic genes from the genomes of Escherichia coli and Acinetobacter baylyi in the presence of the focal nutrient. Pairwise competition experiments with each of 20 mutants auxotrophic for different amino acids, vitamins, and nucleobases against the prototrophic wild type unveiled a pronounced, concentration-dependent growth advantage of around 13% for virtually all mutants tested. Individually deleting different genes from the same biosynthesis pathway entailed gene-specific fitness consequences and loss of the same biosynthetic genes from the genomes of E. coli and A. baylyi differentially affected the fitness of the resulting auxotrophic mutants. Taken together, our findings suggest adaptive benefits could drive the loss of conditionally essential biosynthetic genes. This article is protected by copyright. All rights reserved.Evolution 06/2014; 68(9). DOI:10.1111/evo.12468 · 4.66 Impact Factor
[Show abstract] [Hide abstract]
- "Between F. novicida and F. tularensis, substantial differences are also observed in the ratio of substitution rates at non-synonymous and synonymous sites (dN/dS), with high dN/dS ratios for all F. tularensis branches, and considerably lower ratios for F. novicida (Larsson et al., 2009). Overall, these findings are consistent with the idea that niche restricted bacteria, such as intracellular pathogens, tend to have monomorphic genomes, whereas environmental bacteria are under weaker purifying selection and therefore retain the capacity to adapt to differing conditions by undergoing genomic changes (Moran, 2002; Achtman, 2008; Larsson et al., 2009). "
ABSTRACT: Francisella tularensis is the causative agent of the acute disease tularemia. Due to its extreme infectivity and ability to cause disease upon inhalation, F. tularensis has been classified as a biothreat agent. Two subspecies of F. tularensis, tularensis and holarctica, are responsible for tularemia in humans. In comparison, the closely related species F. novicida very rarely causes human illness and cases that do occur are associated with patients who are immune compromised or have other underlying health problems. Virulence between F. tularensis and F. novicida also differs in laboratory animals. Despite this varying capacity to cause disease, the two species share ~97% nucleotide identity, with F. novicida commonly used as a laboratory surrogate for F. tularensis. As the F. novicida U112 strain is exempt from U.S. select agent regulations, research studies can be carried out in non-registered laboratories lacking specialized containment facilities required for work with virulent F. tularensis strains. This review is designed to highlight phenotypic (clinical, ecological, virulence, and pathogenic) and genomic differences between F. tularensis and F. novicida that warrant maintaining F. novicida and F. tularensis as separate species. Standardized nomenclature for F. novicida is critical for accurate interpretation of experimental results, limiting clinical confusion between F. novicida and F. tularensis and ensuring treatment efficacy studies utilize virulent F. tularensis strains.Frontiers in Cellular and Infection Microbiology 03/2014; 4:35. DOI:10.3389/fcimb.2014.00035 · 2.62 Impact Factor
- "As a consequence, it is plausible that genetic drift (Moran 2002; Marais et al. 2008) has been driving reduction of the Paulinella plastid genome. Consistent with this model (Moran 2002), both the AT content (.60%) and the nucleotide substitution rate of the Paulinella plastid genomes are relatively elevated (Nowack et al. 2008; Yoon et al. 2009). The assumption that a subset of endosymbiont genes have little or no consequences for host fitness would explain why the size of endosymbiont genomes is significantly reduced over short evolutionary periods (Marais et al. 2008; Moran et al. 2009). "