Given the overall modest response in phage 6 populations subjected to strong selection for changes in the UVC survival phenotype, the available evidence strongly suggests that pre-existing constraints prevent the virus from easily adapting. Thus, we did not observe adaptive increases in virus resistance to UV degradation, presumably involving mutagenesis. However, the experimental evolution was of relatively short duration, and additional selection might produce adaptive resistance to UVC damage. Nevertheless, a lack of adaptive response may be unsurprising in phage 6, because elsewhere we showed that genetically robust and brittle strains of the virus generated in the aforementioned MOI experiment did not statistically differ when assayed for UVC survival. 16 Thus, neither direct selection ͑current findings͒ nor indirect selection for robustness against UVC damage was evident in this study system. These observations may be explained by a relatively high level of robustness to UV damage in phage 6, which has already run the gamut of selection, creating a constraint for the virus to improve any further. One ecological explanation may be that the virus naturally infects plant pathogenic bacteria that colonize leaf surfaces, 37 suggesting that prior adaptation to resist UV damage might have precluded observations of further adaptive response in the laboratory.