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Research result overview

A substantial part of my previous research was related to characterisation of resistance to the two bacteriocins, pediocin and nisin, in Listeria monocytogenes. We initiated molecular analysis of mechanisms conferring spontaneously developed resistance using RFDD (restriction fragment differential display), a method that analyses total mRNA without prior knowledge of the genome sequence.

The results showed that pediocin resistance was associated with increased expression of a putative beta-glucoside specific PTS system (Gravesen et al. 2000a), Subsequent investigations showed this was in fact a regulatory consequence, and that high-level resistance to the pediocin-like family of bacteriocins was conferred by one general mechanism involving elimination of a mannose-specific PTS (Gravesen et al., 2002a), specifically by interaction with the MptC component (Ramnath et al., 2004). Low-level resistance could be attributed to several mechanisms (Gravesen et al., 2004, Vadyvaloo et al., 2004).

Nisin resistance was frequently associated with increased expression of a penicillin binding protein (Gravesen et al. 2001), and this change was presumably the direct cause of the phenotype (Gravesen et al., 2004).

We have also investigated the frequencies of bacteriocin resistance development under different environmental conditions (Gravesen et al., 2002b), the influence of growth phase and environmental factors on the efficiency of bacteriocin inactivation (Jydegaard et al., 2000), and whether resistant mutants had reduced growth potential (Gravesen et al., 2002b). The later study showed that although reduced growth rate could be detected in laboratory systems, the mutants had full growth in a food model. Finally, we have analysed cross-resistance between nisin and pediocin (Gravesen et al., 2004), and whether bacteriocin resistance influences virulence gene expression (Gravesen et al., 2004) or sensitivity to antibiotics (Gravesen et al., 2001).

In connection with the above studies, we have compared genotyping methods (Gravesen et al., 2000b), and developed a proteome map for expression studies of L. monocytogenes (Ramnath et al., 2003).