UV hyper‐resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase
Identifieur interne : 000675 ( Istex/Corpus ); précédent : 000674; suivant : 000676UV hyper‐resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase
Auteurs : Marcia S. Osburne ; Brianne M. Holmbeck ; Jorge Frias-Lopez ; Robert Steen ; Katherine Huang ; Libusha Kelly ; Allison Coe ; Kristin Waraska ; Andrew Gagne ; Sallie W. ChisholmSource :
- Environmental Microbiology [ 1462-2912 ] ; 2010-07.
Abstract
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.
Url:
DOI: 10.1111/j.1462-2920.2010.02203.x
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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.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Marcia S. Osburne</name><affiliations><json:string>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</json:string></affiliations></json:item><json:item><name>Brianne M. 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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. 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(+1) 617 253 3310; Fax (+1) 617 258 7009.</p></note><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-2"><persName><forename type="first">Brianne M.</forename><surname>Holmbeck</surname></persName><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-3"><persName><forename type="first">Jorge</forename><surname>Frias‐Lopez</surname></persName><note type="biography">Present address: The Forsyth Institute, 140 The Fenway, Boston, MA 02115, USA.</note><affiliation>Present address: The Forsyth Institute, 140 The Fenway, Boston, MA 02115, USA.</affiliation><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-4"><persName><forename type="first">Robert</forename><surname>Steen</surname></persName><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation></author><author xml:id="author-5"><persName><forename type="first">Katherine</forename><surname>Huang</surname></persName><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-6"><persName><forename type="first">Libusha</forename><surname>Kelly</surname></persName><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-7"><persName><forename type="first">Allison</forename><surname>Coe</surname></persName><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author><author xml:id="author-8"><persName><forename type="first">Kristin</forename><surname>Waraska</surname></persName><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation></author><author xml:id="author-9"><persName><forename type="first">Andrew</forename><surname>Gagne</surname></persName><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation></author><author xml:id="author-10"><persName><forename type="first">Sallie W.</forename><surname>Chisholm</surname></persName><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation></author></analytic><monogr><title level="j">Environmental Microbiology</title><idno type="pISSN">1462-2912</idno><idno type="eISSN">1462-2920</idno><idno type="DOI">10.1111/(ISSN)1462-2920</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-07"></date><biblScope unit="volume">12</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1978">1978</biblScope><biblScope unit="page" to="1988">1988</biblScope></imprint></monogr><idno type="istex">A16CC2963028CA70B351BB49500BE39C9C7E1A8E</idno><idno type="DOI">10.1111/j.1462-2920.2010.02203.x</idno><idno type="ArticleID">EMI2203</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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.</p></abstract></profileDesc><revisionDesc><change when="2010-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A16CC2963028CA70B351BB49500BE39C9C7E1A8E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1462-2920</doi><issn type="print">1462-2912</issn><issn type="electronic">1462-2920</issn><idGroup><id type="product" value="EMI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ENVIRONMENTAL MICROBIOLOGY">Environmental Microbiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="07007"><doi origin="wiley">10.1111/emi.2010.12.issue-7</doi><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2010-07">July 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="15" status="forIssue" accessType="open"><doi origin="wiley">10.1111/j.1462-2920.2010.02203.x</doi><idGroup><id type="unit" value="EMI2203"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="tocHeading1">Research articles</title></titleGroup><copyright>© 2010 Society for Applied Microbiology and Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2010-03-23"></event><event type="publishedOnlineFinalForm" date="2010-07-05"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText source:FullText result:FullText" date="2010-07-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1978">1978</numbering><numbering type="pageLast" number="1988">1988</numbering></numberingGroup><correspondenceTo> E‐mail <email>mosburne@mit.edu</email>; Tel. (+1) 617 253 3310; Fax (+1) 617 258 7009.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EMI.EMI2203.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 14 August, 2009; accepted 28 January, 2010.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="7442"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">UV hyper‐resistance in <i>Prochlorococcus</i> MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase</title><title type="shortAuthors">M. S. Osburne <i>et al.</i></title><title type="short">UV‐hyper‐resist mutants of <i>Prochlorococcus</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Marcia S.</givenNames><familyName>Osburne</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Brianne M.</givenNames><familyName>Holmbeck</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" noteRef="#fn1"><personName><givenNames>Jorge</givenNames><familyName>Frias‐Lopez</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Robert</givenNames><familyName>Steen</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Katherine</givenNames><familyName>Huang</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Libusha</givenNames><familyName>Kelly</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Allison</givenNames><familyName>Coe</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a2"><personName><givenNames>Kristin</givenNames><familyName>Waraska</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a2"><personName><givenNames>Andrew</givenNames><familyName>Gagne</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a1"><personName><givenNames>Sallie W.</givenNames><familyName>Chisholm</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</unparsedAffiliation></affiliation></affiliationGroup><supportingInformation><p><b>Fig. S1.</b> Cell fluorescence following UV treatment is proportional to cell number. Cells from mid‐log phase cultures of MED4 WT and MED4 UVR1 were subjected to 30 s of UV exposure (254 nm) on Day 0, then returned to standard growth conditions. Untreated (?) and UV‐treated (?) cultures were sampled for culture fluorescence (A and B), and for cell number using flow cytometry (C and D). Values are the mean of measurements of duplicate cultures, with error bars showing the standard deviation.</p><p>Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.</p><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:14622912:media:emi2203:EMI_2203_sm_Figure_S1"></mediaResource><caption>Supporting info item</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p>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 <i>Prochlorococcus</i>, we isolated a UV‐hyper‐resistant variant of high light‐adapted strain MED4. The hyper‐resistant strain was constitutively upregulated for expression of the <i>mutT</i>‐<i>phrB</i> 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 <i>mutT</i>‐<i>phrB</i> 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 <i>Prochlorococcus</i> DNA repair mechanisms, genome stability and possibly lysogeny.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label><sup>†</sup></label><p> Present address: The Forsyth Institute, 140 The Fenway, Boston, MA 02115, USA.</p></note><note xml:id="fn2" numbered="no"><p>Re‐use of this article is permitted in accordance with the Terms and Conditions set out at <url href="http://www3.interscience.wiley.com/authorresources/onlineopen.html">http://www3.interscience.wiley.com/authorresources/onlineopen.html</url></p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>UV hyper‐resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>UV‐hyper‐resist mutants of Prochlorococcus</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>UV hyper‐resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase</title></titleInfo><name type="personal"><namePart type="given">Marcia S.</namePart><namePart type="family">Osburne</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><description>Correspondence: E‐mail ; Tel. (+1) 617 253 3310; Fax (+1) 617 258 7009.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brianne M.</namePart><namePart type="family">Holmbeck</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jorge</namePart><namePart type="family">Frias‐Lopez</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><description>Present address: The Forsyth Institute, 140 The Fenway, Boston, MA 02115, USA.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert</namePart><namePart type="family">Steen</namePart><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katherine</namePart><namePart type="family">Huang</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Libusha</namePart><namePart type="family">Kelly</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Allison</namePart><namePart type="family">Coe</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kristin</namePart><namePart type="family">Waraska</namePart><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">Gagne</namePart><affiliation>Biopolymers Facility, Harvard Medical School, Boston, MA 02115, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sallie W.</namePart><namePart type="family">Chisholm</namePart><affiliation>Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-07</dateIssued><edition>Received 14 August, 2009; accepted 28 January, 2010.</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">6</extent><extent unit="tables">3</extent><extent unit="references">39</extent><extent unit="words">7442</extent></physicalDescription><abstract lang="en">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.</abstract><relatedItem type="host"><titleInfo><title>Environmental Microbiology</title></titleInfo><genre type="journal">journal</genre><note type="content"> Fig. S1. Cell fluorescence following UV treatment is proportional to cell number. Cells from mid‐log phase cultures of MED4 WT and MED4 UVR1 were subjected to 30 s of UV exposure (254 nm) on Day 0, then returned to standard growth conditions. Untreated (?) and UV‐treated (?) cultures were sampled for culture fluorescence (A and B), and for cell number using flow cytometry (C and D). Values are the mean of measurements of duplicate cultures, with error bars showing the standard deviation. Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. Fig. S1. Cell fluorescence following UV treatment is proportional to cell number. Cells from mid‐log phase cultures of MED4 WT and MED4 UVR1 were subjected to 30 s of UV exposure (254 nm) on Day 0, then returned to standard growth conditions. Untreated (?) and UV‐treated (?) cultures were sampled for culture fluorescence (A and B), and for cell number using flow cytometry (C and D). Values are the mean of measurements of duplicate cultures, with error bars showing the standard deviation. Please note: Wiley‐Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. 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