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and ecological factors that are specific to the bacteria and habitats involved.

There are other conditions that may favor the infectious transfer of accessory elements as well. For example, a number of characters expressed by bacteria of one lineage augment the fitness of bacteria of other lineages in their vicinity whether the beneficiaries carry those genes that code for that character or not. Examples include the production of secreted agents that kill competing bacterial species (e.g., antibiotics and bacteriocins) and somatic cells (e.g., toxins) and those that detoxify or condition the local environment for bacterial growth (e.g., β-lactamases and other enzymes that denature antibiotics exogenously; Lenski and Hattingh, 1986). One consequence is that bacteria not carrying these genes can free-ride on the efforts of those that do. In such cases, infectious gene transfer would provide a way to convert these “cheaters” into good citizens that share the burden as well as the advantages of carrying and expressing these genes (Smith, 2000).

Evolving to Evolve: The Evolution of Infectious Gene Transfer

Thus far, we have considered the mechanisms that can maintain infectiously transmitted genetic elements over evolutionary time. But how did these mechanisms and the capacity for acquisition of genes from without evolve in the first place? We believe that, for accessory genetic elements, the most parsimonious (and possibly even correct) answers to these questions are those that treat the individual genetic elements, rather than their hosts, as the objects of natural selection.

Infectious Gene Transfer as a Product of Coincidental Evolution?

A number of years ago, Richard Lenski and B.R.L. (Levin, 1988; Levin and Lenski, 1983) considered the mechanisms responsible for conjugative plasmids and phages to serve as vehicles (vectors) for the infectious transfer of host genes: plasmid-mediated conjugation and phage-mediated transduction. They postulated that these forms of bacterial sex are coincidental to the infectious transfer of the elements themselves and to the presence of recombination repair enzymes in their host bacteria. Although we are now in a new and doubtless more enlightened millennium, this coincidental evolution hypothesis remains plausible and parsimonious, albeit still not formally tested. Clearly, generalized transduction and plasmid-mediated recombination (such as that by the F+ plasmid of E. coli K-12) are to the disadvantage of the phage and plasmid, respectively. Coincidental evolution also seems a reasonable hypothesis for the propensity of conjugative plasmids and bacteriophages to pick up hitchhik



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