INTRODUCTION

Evolution of catabolic pathways in bacteria is most often equivalent to ‘catabolic pathway expansion’ or ‘new acquisition of catabolic properties’, although in essence it could also mean loss or deletion. Even if we limit ourselves to this narrow interpretation, changes in the repertoire of catabolic functions of a bacterium are largely attributable to the activity of mobile genetic elements (van der Meer, 1997, 2002). Typically, mobile genetic elements may create new recombinations between previously disconnected DNA fragments, even from different bacterial origins, thus assembling bits and pieces together. Such recombinations are not necessarily needed to result in a single, smoothly transcribed new operon; any workable gene or fragment of genes within the boundaries of the new host cell may contribute to the catabolic expansion of functions (Dogra et al., 2004; Müller et al., 2004). Classical examples of evolutionarily ancient pathway expansions are the formation of the operons for toluene and xylene degradation in pseudomonads (Harayama et al., 1987; Harayama & Rekik, 1993; Greated et al., 2002). Observations of (most likely) very recent pathway expansions include the formation of pathways for chlorobenzene degradation, such as in Pseudomonas sp. strain P51 (van der Meer et al., 1991) and Ralstonia sp. strain JS705 (van der Meer et al., 1998; Müller et al., 2003), or pathways for 2,4-dichloro-phenoxyacetic acid degradation in Ralstonia eutropha (now Cupriavidus necator) JMP134 (Laemmli et al., 2000; Trefault et al., 2004).