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dc.contributor.authorHolmbeck, Brianne M.
dc.contributor.authorOsburne, Marcia
dc.contributor.authorFrias-Lopez, Jorge
dc.contributor.authorHuang, Katherine H.
dc.contributor.authorChisholm, Sallie (Penny)
dc.contributor.authorKelly, Libusha
dc.contributor.authorCoe, Allison
dc.contributor.authorSteen, Robert
dc.contributor.authorWaraska, Kristin
dc.contributor.authorGagne, Andrew
dc.date.accessioned2011-02-22T18:25:10Z
dc.date.available2011-02-22T18:25:10Z
dc.date.issued2010-07
dc.identifier.issn1462-2920
dc.identifier.issn1462-2912
dc.identifier.urihttp://hdl.handle.net/1721.1/61006
dc.description.abstractExposure 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.en_US
dc.description.sponsorshipGordon and Betty Moore Foundationen_US
dc.description.sponsorshipUnited States. Dept. of Energy. Genomics:GTLen_US
dc.description.sponsorshipNational Science Foundation (U.S.)en_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.description.sponsorshipCameron and Hayden Lord Foundationen_US
dc.language.isoen_US
dc.publisherSociety for Applied Microbiology / Blackwellen_US
dc.relation.isversionofhttp://dx.doi.org/10.1111/j.1462-2920.2010.02203.xen_US
dc.rightsAttribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourceProf. Chisholm via Anne Grahamen_US
dc.titleUV hyper-resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyaseen_US
dc.typeArticleen_US
dc.identifier.citationOsburne, Marcia S. et al. “UV hyper-resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase.” Environmental Microbiology 12.7 (2010): 1978-1988. © 2010 Society for Applied Microbiology and Blackwell Publishing Ltden_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Civil and Environmental Engineeringen_US
dc.contributor.approverChisholm, Sallie (Penny)
dc.contributor.mitauthorOsburne, Marcia
dc.contributor.mitauthorHolmbeck, Brianne M.
dc.contributor.mitauthorFrias-Lopez, Jorge
dc.contributor.mitauthorHuang, Katherine H.
dc.contributor.mitauthorKelly, Libusha
dc.contributor.mitauthorCoe, Allison
dc.contributor.mitauthorChisholm, Sallie (Penny)
dc.relation.journalENVIRONMENTAL MICROBIOLOGYen_US
dc.eprint.versionOriginal manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
dspace.orderedauthorsOsburne, Marcia S.; Holmbeck, Brianne M.; Frias-Lopez, Jorge; Steen, Robert; Huang, Katherine; Kelly, Libusha; Coe, Allison; Waraska, Kristin; Gagne, Andrew; Chisholm, Sallie W.en
dc.identifier.orcidhttps://orcid.org/0000-0003-1072-6828
mit.licenseOPEN_ACCESS_POLICYen_US
mit.metadata.statusComplete


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