The PFGE gave the greatest discriminatory power. Indeed PFGE gave profiles for different strains that by another way were grouped together in MSTrees. For example, ST2 (Figure 3) comprised low-virulence strains of the phenotypic Groups-I,

-V, and -VI, which had different PFGE profiles. www.selleckchem.com/products/anlotinib-al3818.html Similarly, the low-virulence strains AF105 and LSEA-99-23 exhibited the same MLST profile but had distinct profiles in PFGE. Interestingly, MSTree identified specific ST for half of the low-virulence strains belonging to lineage II. Overall, we identified low-virulence L. monocytogenes strains in both lineages I and II. No hypothesis could be advanced for the lineage III/IV, as they were few strains studied here represented these lineages. Our population structure showed that low-virulence strains are linked firstly according to their lineage, then to their serotypes and after which, they lost their virulence suggesting

a relatively recent emergence. MSTree analyses showed that low-virulence strains belonging to lineage II formed a tightly clustered, monophyletic group with limited diversity, in contrast to the low-virulence strains of lineage I. All our observations further supported the fact that some correlations existed between virulence level and point mutations, base substitutions inducing a stop-codon, or A-1210477 datasheet inactivation of different virulence proteins, rather selleckchem than on horizontal transfer or gene loss [7, 8, 20]. A characteristic of lineage II low-virulence Protein tyrosine phosphatase strains was that all strains had a point mutation in the virulence inlA gene. Interestingly, there was a strong correlation between the inlA mutation and the genotypic group which were based on the mutations responsible for the virulence lost. Moreover, all strains of ST31 had only two

different inlA mutations, but only the strains with the mutation type 5, according to Van Stelten also have the PrfAK220T mutation [17]. This observation suggested that the inlA mutation appeared before the prfA mutation. Regardless of the nature of mutations in inlA in the different low-virulence strains, there was clearly a link between their prevalence in food environments and the inlA mutations. Indeed, the inlA mutations were identified mainly in serotypes 1/2a and 1/2c from lineage II isolated from food and food-processing environments [17, 21]. As such, it is reasonable to hypothesize that variations within these groups have been shaped to a greater extent by selective constraints operating in food manufacturing-plants. It is intriguing that InlA, and to a lesser extent PrfA, which are important bacterial factors for host colonization, were lost. This pattern could be explained either by relaxation of the selective constraint to maintain InlA and PrfA function or by a selective advantage provided by the loss of functional virulence proteins in the ecological niche occupied by these strains.