The investigators took a monoclonal culture of a bacterium which was penicillin resistant, thanks to the enzyme penicillinase. They exposed the culture to a mutagen and to another antibiotic, I think erythromycin, to which the bacterium was originally not resistant. Most of the bacteria died off, but the remaining living and multiplying bacteria were found now to be erythromycin resistant. Note that the monoclonality means there were no resistant bacteria originally there in the population; all of the original, pre-mutagen bacteria were genetically identical.
When they investigated the penicllinase gene of the newly resistant bacterium, what they found was a single DNA base change, located at the site of the antibiotic binding pocket of penicillinase, which 'loosened' the pocket, allowing it to bind erthyromycin, which was then hydrolysed. This change somewhat lowered the activity towards penicillin, but a few more cycles of exposure to both antibiotics introduced another mutation which gave a 'better' pocket, as active as the original enzyme to penicillin, but able additionally to hydrolyse erthyromycin. The second mutation was located and identified.
The bacterium had clearly evolved a new functionality, without loss of the old one, by mutation and natural selection. There is no doubt the same change would have happened, albeit much more slowly, by natural mutation; there is no doubt the selection would have happened in the wild if the bug were exposed to two different antibiotics. Development of new antibiotic resistance in the wild is well-documented, and it follows the same pattern of point mutation as was described in this paper.
As it happens, it is likely most new functionalities don't follow this pattern; they more likely happen by gene duplication. Once you have two identical genes, one can mutate and go do something else, while the other maintains the original function.
Well I guess that just goes to show you, Professor, that among the population of monoclonal (genetically identical) bacteria, for whatever reason, perhaps some of these "critturs" were more successful information processors than others. Perhaps something in the cloning process (an "artificial" albeit human intelligent intervention) may account for this -- do we really know whether or not this might be the case? I mean, sone rather unexpected things have been observed to have happened to "monoclonal" higher-order animals -- check out the history of the famous Dolly. And because they were (hypothetically) better/more efficient readers of the "code" than the ones the intervention destroyed, they then became subject to the Darwinist selection mechanism -- meaning they improved their chances at survivability because they managed to acquire new functionality -- resistance to erythromycin -- while not losing old functionality -- resistance to penicillin. There is nothing that I know of that argues that "new" functionality must come at the expense of losing "old" functionality. Isn't this what evolution is supposed to be all about?
I have an experiment, too, to run by you, for your comment. But it'll have to wait for tomorrow, since I left my source materials at the office today, and don't have as good a memory as you.