Abstract
SidJ is a Dot/Icm effector involved in the trafficking or retention of ER-derived vesicles to Legionella pneumophila vacuoles whose mutation causes an observable growth defect, both in macrophage and amoeba hosts. Given the crucial role of this effector in L. pneumophila virulence we investigated the mechanisms shaping its molecular evolution. The alignment of SidJ sequences revealed several alleles with amino acid variations that may influence the protein properties. The identification of HGT events and the detection of balancing selection operating on sidJ evolution emerge as a clear result. Evidence suggests that intragenic recombination is an important strategy in the evolutionary adaptive process playing an active role on sidJ genetic plasticity. This pattern of evolution is in accordance with the life style of L. pneumophila as a broad host-range pathogen by preventing host-specialization and contributing to the resilience of the species.
Highlights
Legionella pneumophila is a ubiquitous bacterium in freshwater environments as well as in many man-made water systems worldwide known for its ability to cause pneumonia in humans [1]
A similar significant evolutionary drift was observed for the strain Lansing 3, that belonged to cluster rpoB-B with all other L. pneumophila subsp. fraseri strains, since it was grouped in a distinct cluster in the Maximum likelihood (ML) tree inferred from the sidJ gene along with other L. pneumophila subsp. pneumophila strains (Table 1)
The detection of intragenic recombination events, within a gene, in opposition to intergenic recombination events, between genes, in L. pneumophila has been rarely reported it is worth noticing that we have found that this form of recombination has a fundamental role on the molecular evolution of L. pneumophila genes critical for virulence, namely in the dotA gene [18] and in sidJ
Summary
Legionella pneumophila is a ubiquitous bacterium in freshwater environments as well as in many man-made water systems worldwide known for its ability to cause pneumonia in humans [1]. The long-term co-evolution of L. pneumophila with free-living amoebae has influenced the genomic structure of this organism since amoeba may act as a gene melting pot, allowing diverse microorganisms to evolve by gene acquisition and loss, and either adapt to the intra-amoebal lifestyle or evolve into new pathogenic forms [8,10,11,12]. This lifestyle, namely the interaction with different protozoan in different environments, may have prevented host-specialization and be responsible for the evolutionary story of L. pneumophila [13]. This evidence supports the hypothesis proposed by Coscollaand Gonzalez-Candelas [16] that isolates of L. pneumophila recovered from clinical cases are a limited, non-random subset of all genotypes existing in nature, perhaps representing an especially adapted group of clones
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