Exposure to solar radiation can cause mortality in natural communities of 
pico-phytoplankton, both at the surface and to a depth of at least 30 m. DNA 
damage is a significant cause of death, mainly due to cyclobutane pyrimidine 
dimer formation, which can be lethal if not repaired. While developing a UV 
mutagenesis protocol for the marine cyanobacterium Prochlorococcus, we isolated 
a UV-hyper-resistant variant of high light-adapted strain MED4. The 
hyper-resistant strain was constitutively upregulated for expression of the 
mutT-phrB operon, encoding nudix hydrolase and photolyase, both of which are 
involved in repair of DNA damage that can be caused by UV light. Photolyase 
(PhrB) breaks pyrimidine dimers typically caused by UV exposure, using energy 
from visible light in the process known as photoreactivation. Nudix hydrolase 
(MutT) hydrolyses 8-oxo-dGTP, an aberrant form of GTP that results from 
oxidizing conditions, including UV radiation, thus impeding mispairing and 
mutagenesis by preventing incorporation of the aberrant form into DNA. These 
processes are error-free, in contrast to error-prone SOS dark repair systems 
that are widespread in bacteria. The UV-hyper-resistant strain contained only a 
single mutation: a 1 bp deletion in the intergenic region directly upstream of 
the mutT-phrB operon. Two subsequent enrichments for MED4 UV-hyper-resistant 
strains from MED4 wild-type cultures gave rise to strains containing this same 1 
bp deletion, affirming its connection to the hyper-resistant phenotype. These 
results have implications for Prochlorococcus DNA repair mechanisms, genome 
stability and possibly lysogeny.