Data from experiments with single-stranded vectors that carry a site-s
pecific cyclobutane dimer, pyrimidine (6-4) pyrimidone adduct, or abas
ic lesion, replicated in either E. coli or, in some cases, bakers' yea
st, Saccharomyces cerevisiae, are used to examine two questions: (i) w
hat factors are responsible for the lesion's mutagenicity? and (ii) wh
at are the relative contributions of different photoproducts to the sp
ectrum of UV-induced mutations? With respect to the first question, we
suggest that the structure of the mutagen-modified template itself la
rgely determines the kinds of mutations induced, but the relative freq
uencies of these mutations, the error frequency, and the bypass freque
ncy are strongly dependent on the particular organism studied. With re
spect to the second question, we suggest that cyclobutane dimers may b
e responsible for most of the mutations in slowly replicating genomes
because of the deamination of cytosine, and that the T-T, and to a les
ser extent the T-C, (6-4) adducts play a greater role in the UV mutage
nesis of quickly replicating viruses, such as M13 and lambda phage.