Transient Accumulation of Okazaki Fragments as a Result of Uracil Incorporation into Nascent DNA
Strains of Escherichia coli with a mutation in the sof (dnaS) locus show a higher than normal frequency of recombination (are hyper rec) and incorporate label into short (4-5S) DNA fragments following brief [3H]thymidine pulses [Konrad and Lehman, Proc. Natl. Acad. Sci. USA 72, 2150 (1975)]. These m...
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Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1977-01, Vol.74 (1), p.154-157 |
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description | Strains of Escherichia coli with a mutation in the sof (dnaS) locus show a higher than normal frequency of recombination (are hyper rec) and incorporate label into short (4-5S) DNA fragments following brief [3H]thymidine pulses [Konrad and Lehman, Proc. Natl. Acad. Sci. USA 72, 2150 (1975)]. These mutant strains have now been found to be defective in deoxyuridinetriphosphate diphosphohydrolase (dUTPase; deoxyuridinetriphosphatase, EC 3.6.1.23), the enzyme that catalyzes the hydrolysis of dUTP to dUMP and PPi. Reversion of one sof-mutation to sof+restores dUTPase activity and abolishes the accumulation of labeled 4-5S DNA fragments. Mutants initially isolated as defective in dUTPase (dut-) are also hyper rec and show transient accumulation of short DNA fragments. Both the sof and dut mutations are located at 81 min on the E. coli map, closely linked to the pyrE locus. The sof and dut loci thus appear to be identical. A decrease in dUTPase as a consequence of a sof or dut mutation may result in the increased incorporation of uracil into DNA. Rapid removal of the uracil by an excision-repair process could then lead to the transient accumulation of short DNA fragments. It is possible that at least a portion of the Okazaki fragments seen in wild-type cells may originate in this way. |
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R. ; Hochhauser, Steven ; Weiss, Bernard</creator><creatorcontrib>Tye, Bik-Kwoon ; Nyman, Per-Olof ; Lehman, I. R. ; Hochhauser, Steven ; Weiss, Bernard</creatorcontrib><description>Strains of Escherichia coli with a mutation in the sof (dnaS) locus show a higher than normal frequency of recombination (are hyper rec) and incorporate label into short (4-5S) DNA fragments following brief [3H]thymidine pulses [Konrad and Lehman, Proc. Natl. Acad. Sci. USA 72, 2150 (1975)]. These mutant strains have now been found to be defective in deoxyuridinetriphosphate diphosphohydrolase (dUTPase; deoxyuridinetriphosphatase, EC 3.6.1.23), the enzyme that catalyzes the hydrolysis of dUTP to dUMP and PPi. Reversion of one sof-mutation to sof+restores dUTPase activity and abolishes the accumulation of labeled 4-5S DNA fragments. Mutants initially isolated as defective in dUTPase (dut-) are also hyper rec and show transient accumulation of short DNA fragments. Both the sof and dut mutations are located at 81 min on the E. coli map, closely linked to the pyrE locus. The sof and dut loci thus appear to be identical. A decrease in dUTPase as a consequence of a sof or dut mutation may result in the increased incorporation of uracil into DNA. Rapid removal of the uracil by an excision-repair process could then lead to the transient accumulation of short DNA fragments. It is possible that at least a portion of the Okazaki fragments seen in wild-type cells may originate in this way.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.74.1.154</identifier><identifier>PMID: 319455</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Biochemistry ; Centrifugation ; Chromosome Mapping ; Deoxyuridine ; Diploidy ; DNA ; DNA Repair ; DNA Replication ; DNA, Bacterial - metabolism ; Enzymes ; Escherichia coli ; Genes ; Genetic loci ; Genetic mutation ; Laboratory schools ; Molecular Weight ; Mutation ; Phenotypes ; Pyrophosphatases - deficiency ; Pyrophosphatases - metabolism ; Recombination, Genetic ; Uracil Nucleotides - metabolism</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1977-01, Vol.74 (1), p.154-157</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-3b9992379bdf9b02c1b16c79ee4e7979e0332901d5a1efd58c31249d5b7925153</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/74/1.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/66533$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/66533$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/319455$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tye, Bik-Kwoon</creatorcontrib><creatorcontrib>Nyman, Per-Olof</creatorcontrib><creatorcontrib>Lehman, I. R.</creatorcontrib><creatorcontrib>Hochhauser, Steven</creatorcontrib><creatorcontrib>Weiss, Bernard</creatorcontrib><title>Transient Accumulation of Okazaki Fragments as a Result of Uracil Incorporation into Nascent DNA</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Strains of Escherichia coli with a mutation in the sof (dnaS) locus show a higher than normal frequency of recombination (are hyper rec) and incorporate label into short (4-5S) DNA fragments following brief [3H]thymidine pulses [Konrad and Lehman, Proc. Natl. Acad. Sci. USA 72, 2150 (1975)]. These mutant strains have now been found to be defective in deoxyuridinetriphosphate diphosphohydrolase (dUTPase; deoxyuridinetriphosphatase, EC 3.6.1.23), the enzyme that catalyzes the hydrolysis of dUTP to dUMP and PPi. Reversion of one sof-mutation to sof+restores dUTPase activity and abolishes the accumulation of labeled 4-5S DNA fragments. Mutants initially isolated as defective in dUTPase (dut-) are also hyper rec and show transient accumulation of short DNA fragments. Both the sof and dut mutations are located at 81 min on the E. coli map, closely linked to the pyrE locus. The sof and dut loci thus appear to be identical. A decrease in dUTPase as a consequence of a sof or dut mutation may result in the increased incorporation of uracil into DNA. Rapid removal of the uracil by an excision-repair process could then lead to the transient accumulation of short DNA fragments. It is possible that at least a portion of the Okazaki fragments seen in wild-type cells may originate in this way.</description><subject>Biochemistry</subject><subject>Centrifugation</subject><subject>Chromosome Mapping</subject><subject>Deoxyuridine</subject><subject>Diploidy</subject><subject>DNA</subject><subject>DNA Repair</subject><subject>DNA Replication</subject><subject>DNA, Bacterial - metabolism</subject><subject>Enzymes</subject><subject>Escherichia coli</subject><subject>Genes</subject><subject>Genetic loci</subject><subject>Genetic mutation</subject><subject>Laboratory schools</subject><subject>Molecular Weight</subject><subject>Mutation</subject><subject>Phenotypes</subject><subject>Pyrophosphatases - deficiency</subject><subject>Pyrophosphatases - metabolism</subject><subject>Recombination, Genetic</subject><subject>Uracil Nucleotides - metabolism</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1977</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUFP3DAQhS3Ulm63PfZS9ZAL3LK1YzuJDz2sli6shECq4GwcxwGDE6e2g4BfX0dZVssFzUhzeN-bsfUA-I7gAsEC_-o74RcFWaAFouQAzBBkKM0Jgx_ADMKsSEuSkc_gi_f3EEJGS3gIPmHECKUzcHPlROe16kKylHJoByOCtl1im-TyQbyIB52snbhtI-ATETv5q_xgwghcOyG1STadtK63bjLqLtjkQng5rjy5WH4FHxthvPq2nXNwvf5ztTpLzy9PN6vleSoJhSHFFWMswwWr6oZVMJOoQrksmFJEFSxOiHHGIKqpQKqpaSkxygiraVWwjCKK5-D3tLcfqlbV43knDO-dboV75lZo_lbp9B2_tY8cM5yhPPqPt35n_w3KB97q-AljRKfs4HmJY5URnoN0AqWz3jvV7G4gyMdA-BgILwhHPAYS-Z_7D9vRUwJ78uh6FffcR-_IvBmMCeopRO7HxN37YN0OzHOKMf4PLs-n4Q</recordid><startdate>19770101</startdate><enddate>19770101</enddate><creator>Tye, Bik-Kwoon</creator><creator>Nyman, Per-Olof</creator><creator>Lehman, I. R.</creator><creator>Hochhauser, Steven</creator><creator>Weiss, Bernard</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19770101</creationdate><title>Transient Accumulation of Okazaki Fragments as a Result of Uracil Incorporation into Nascent DNA</title><author>Tye, Bik-Kwoon ; Nyman, Per-Olof ; Lehman, I. R. ; Hochhauser, Steven ; Weiss, Bernard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-3b9992379bdf9b02c1b16c79ee4e7979e0332901d5a1efd58c31249d5b7925153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1977</creationdate><topic>Biochemistry</topic><topic>Centrifugation</topic><topic>Chromosome Mapping</topic><topic>Deoxyuridine</topic><topic>Diploidy</topic><topic>DNA</topic><topic>DNA Repair</topic><topic>DNA Replication</topic><topic>DNA, Bacterial - metabolism</topic><topic>Enzymes</topic><topic>Escherichia coli</topic><topic>Genes</topic><topic>Genetic loci</topic><topic>Genetic mutation</topic><topic>Laboratory schools</topic><topic>Molecular Weight</topic><topic>Mutation</topic><topic>Phenotypes</topic><topic>Pyrophosphatases - deficiency</topic><topic>Pyrophosphatases - metabolism</topic><topic>Recombination, Genetic</topic><topic>Uracil Nucleotides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tye, Bik-Kwoon</creatorcontrib><creatorcontrib>Nyman, Per-Olof</creatorcontrib><creatorcontrib>Lehman, I. R.</creatorcontrib><creatorcontrib>Hochhauser, Steven</creatorcontrib><creatorcontrib>Weiss, Bernard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tye, Bik-Kwoon</au><au>Nyman, Per-Olof</au><au>Lehman, I. R.</au><au>Hochhauser, Steven</au><au>Weiss, Bernard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transient Accumulation of Okazaki Fragments as a Result of Uracil Incorporation into Nascent DNA</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1977-01-01</date><risdate>1977</risdate><volume>74</volume><issue>1</issue><spage>154</spage><epage>157</epage><pages>154-157</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Strains of Escherichia coli with a mutation in the sof (dnaS) locus show a higher than normal frequency of recombination (are hyper rec) and incorporate label into short (4-5S) DNA fragments following brief [3H]thymidine pulses [Konrad and Lehman, Proc. Natl. Acad. Sci. USA 72, 2150 (1975)]. These mutant strains have now been found to be defective in deoxyuridinetriphosphate diphosphohydrolase (dUTPase; deoxyuridinetriphosphatase, EC 3.6.1.23), the enzyme that catalyzes the hydrolysis of dUTP to dUMP and PPi. Reversion of one sof-mutation to sof+restores dUTPase activity and abolishes the accumulation of labeled 4-5S DNA fragments. Mutants initially isolated as defective in dUTPase (dut-) are also hyper rec and show transient accumulation of short DNA fragments. Both the sof and dut mutations are located at 81 min on the E. coli map, closely linked to the pyrE locus. The sof and dut loci thus appear to be identical. A decrease in dUTPase as a consequence of a sof or dut mutation may result in the increased incorporation of uracil into DNA. Rapid removal of the uracil by an excision-repair process could then lead to the transient accumulation of short DNA fragments. It is possible that at least a portion of the Okazaki fragments seen in wild-type cells may originate in this way.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>319455</pmid><doi>10.1073/pnas.74.1.154</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biochemistry Centrifugation Chromosome Mapping Deoxyuridine Diploidy DNA DNA Repair DNA Replication DNA, Bacterial - metabolism Enzymes Escherichia coli Genes Genetic loci Genetic mutation Laboratory schools Molecular Weight Mutation Phenotypes Pyrophosphatases - deficiency Pyrophosphatases - metabolism Recombination, Genetic Uracil Nucleotides - metabolism |
title | Transient Accumulation of Okazaki Fragments as a Result of Uracil Incorporation into Nascent DNA |
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