The term "Genomics", coined by Thomas Roderick in 1986, refers to an at-that-time new scientific discipline of mapping, sequencing, and analyzing genomes (Kuska 1998). Although genomics was the object of controversies in its early times, it was boosted by the human genome project and has meanwhile revolutionized our way of thinking in biological research. Given the small size of their genomes, this is particularly true for bacteria. Genomics also provides, for the first time, the possibility to analyze at the molecular level an organism as an entity, and with the emergence of systems biology it will be possible to integrate all different knowledge coherently. However, genomics is still intricately linked to genetics, a discipline developed in the 19th century. With respect to the genus Listeria, genomics started with the first chromosome structure analysis based on pulsed field gel electrophoresis (PFGE) and has led now to what is referred to as postgenomics studies including systematic gene knockouts, proteome, and transcriptome analysis.
The first published description of L. monocytogenes was that by Murray et al. in 1926. These researchers observed six cases of rather sudden death of young rabbits in 1924 in the animal-breeding establishment of the Department of Pathology of Cambridge and many more in the succeeding 15 months. The interesting characters presented by the disease and the mortality prompted investigation. In 1927, during investigations of unusual deaths observed in gerbils near Johannesburg (South Africa), Pirie discovered the same organism (Pirie 1927). Since then many studies have been undertaken to characterize L. monocytogenes which was until 1966 the only member of the genus. Listeria are Gram-positive rods that are not considered as naturally competent and, although phages infecting Listeria have been known for a long time, general transduction systems were described only in 2000 (Hodgson 2000). Due to the absence of genetic tools, L. monocytogenes, like most pathogenic bacteria, escaped classical genetics. Nevertheless, the development of transposon mutagenesis and genetic screens allowed the isolation of mutants affected in virulence genes. The first gene to be inactivated was hly encoding the cytolysin, by using the 26-kb-long transposon Tn1545 (Gaillard et al. 1986). The loss of virulence associated with the inactivation of this gene demonstrated the critical role of hemolysin in virulence. Following hly, major virulence determinants, most of them encoded on the so-called "virulence gene cluster" as well as on the inlAB operon, were subsequently identified by using various phenotypic tests and transposon mutant collections (Portnoy et al. 1992). Genetic identification of virulence factors depends heavily on the experimental approach used to test for virulence. For example, signature tagged mutagenesis (STM), by testing pools of mutants, allows screening of a large number of mutant strains in an animal model. Recently, several STM screens have been performed with L. monocytogenes leading to the identification of additional virulence factors including regulatory systems like the two-component system Lgr, a homolog of the Staphylococcus aureus Agr system (Autret et al. 2003) and the VirR response regulator (Mandin et al. 2005a). However, genomics of L. monocytogenes was the prerequisite to gain a complete understanding of the genetic basis of the virulence and the ecology of this food-borne pathogen.
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