Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair
The Mre11 and Pso2 nucleases function in homologous recombination and interstrand cross-link (ICL) repair pathways, respectively, while the Exo1 nuclease is involved in homologous recombination and mismatch repair. Characterization of the sensitivity of single, double and triple mutants for these nu...
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| Veröffentlicht in: | DNA repair 2008-04, Vol.7 (4), p.655-662 |
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| creator | Lam, Alicia F. Krogh, Berit O. Symington, Lorraine S. |
| description | The Mre11 and Pso2 nucleases function in homologous recombination and interstrand cross-link (ICL) repair pathways, respectively, while the Exo1 nuclease is involved in homologous recombination and mismatch repair. Characterization of the sensitivity of single, double and triple mutants for these nucleases in
Saccharomyces cerevisiae to various DNA damaging agents reveals complex interactions that depend on the type of DNA damage. The
pso2 mutant is uniquely sensitive to agents that generate ICLs and
mre11-H125N shows the highest sensitivity of the single mutants for ionizing radiation and methyl methane sulfonate. However, elimination of all three nucleases confers higher sensitivity to IR than any of the single or double mutant combinations indicating a high degree of redundancy and versatility in the response to DNA damage. In response to ICL agents, double-strand breaks are still formed in the triple nuclease mutant indicating that none of these nucleases are responsible for unhooking cross-links. |
| doi_str_mv | 10.1016/j.dnarep.2007.12.014 |
| format | Article |
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Saccharomyces cerevisiae to various DNA damaging agents reveals complex interactions that depend on the type of DNA damage. The
pso2 mutant is uniquely sensitive to agents that generate ICLs and
mre11-H125N shows the highest sensitivity of the single mutants for ionizing radiation and methyl methane sulfonate. However, elimination of all three nucleases confers higher sensitivity to IR than any of the single or double mutant combinations indicating a high degree of redundancy and versatility in the response to DNA damage. In response to ICL agents, double-strand breaks are still formed in the triple nuclease mutant indicating that none of these nucleases are responsible for unhooking cross-links.</description><identifier>ISSN: 1568-7864</identifier><identifier>EISSN: 1568-7856</identifier><identifier>DOI: 10.1016/j.dnarep.2007.12.014</identifier><identifier>PMID: 18295552</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Bacteriology ; Biological and medical sciences ; DNA Damage ; DNA Repair ; Endodeoxyribonucleases - genetics ; Endodeoxyribonucleases - metabolism ; Exo1 ; Exodeoxyribonucleases - genetics ; Exodeoxyribonucleases - metabolism ; Fundamental and applied biological sciences. Psychology ; Gamma Rays ; Growth, nutrition, cell differenciation ; Homologous recombination ; Interstrand cross-links ; Methyl Methanesulfonate - toxicity ; Microbiology ; Molecular and cellular biology ; Molecular genetics ; Mre11 ; Mutagenesis. Repair ; Mutagens - toxicity ; Pso2 ; Radiation Tolerance - genetics ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - drug effects ; Saccharomyces cerevisiae - enzymology ; Saccharomyces cerevisiae - genetics ; Saccharomyces cerevisiae - radiation effects ; Saccharomyces cerevisiae Proteins - genetics ; Saccharomyces cerevisiae Proteins - metabolism</subject><ispartof>DNA repair, 2008-04, Vol.7 (4), p.655-662</ispartof><rights>2008 Elsevier B.V.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-e5d37c2520424c3235175aa8ac0e262dfee5c40e2c3f274612ea0f1330953a83</citedby><cites>FETCH-LOGICAL-c523t-e5d37c2520424c3235175aa8ac0e262dfee5c40e2c3f274612ea0f1330953a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1568786408000050$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20237961$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18295552$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lam, Alicia F.</creatorcontrib><creatorcontrib>Krogh, Berit O.</creatorcontrib><creatorcontrib>Symington, Lorraine S.</creatorcontrib><title>Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair</title><title>DNA repair</title><addtitle>DNA Repair (Amst)</addtitle><description>The Mre11 and Pso2 nucleases function in homologous recombination and interstrand cross-link (ICL) repair pathways, respectively, while the Exo1 nuclease is involved in homologous recombination and mismatch repair. Characterization of the sensitivity of single, double and triple mutants for these nucleases in
Saccharomyces cerevisiae to various DNA damaging agents reveals complex interactions that depend on the type of DNA damage. The
pso2 mutant is uniquely sensitive to agents that generate ICLs and
mre11-H125N shows the highest sensitivity of the single mutants for ionizing radiation and methyl methane sulfonate. However, elimination of all three nucleases confers higher sensitivity to IR than any of the single or double mutant combinations indicating a high degree of redundancy and versatility in the response to DNA damage. In response to ICL agents, double-strand breaks are still formed in the triple nuclease mutant indicating that none of these nucleases are responsible for unhooking cross-links.</description><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>Endodeoxyribonucleases - genetics</subject><subject>Endodeoxyribonucleases - metabolism</subject><subject>Exo1</subject><subject>Exodeoxyribonucleases - genetics</subject><subject>Exodeoxyribonucleases - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gamma Rays</subject><subject>Growth, nutrition, cell differenciation</subject><subject>Homologous recombination</subject><subject>Interstrand cross-links</subject><subject>Methyl Methanesulfonate - toxicity</subject><subject>Microbiology</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mre11</subject><subject>Mutagenesis. Repair</subject><subject>Mutagens - toxicity</subject><subject>Pso2</subject><subject>Radiation Tolerance - genetics</subject><subject>Saccharomyces cerevisiae</subject><subject>Saccharomyces cerevisiae - drug effects</subject><subject>Saccharomyces cerevisiae - enzymology</subject><subject>Saccharomyces cerevisiae - genetics</subject><subject>Saccharomyces cerevisiae - radiation effects</subject><subject>Saccharomyces cerevisiae Proteins - genetics</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><issn>1568-7864</issn><issn>1568-7856</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhSMEoqXwDxDyhq6YYF_HdrJBqkp5SOWxGNbWxblpPcrYwU5G8O9xmdEUNqx8JX_3-PicqnoueC240K83dR8w0VQD56YWUHPRPKhOhdLtyrRKPzzOujmpnuS84Vwoo_Xj6kS00Cml4LRafwv-x0IMQ8_ijtKI0-TDDRuW4GYfQ2ZxYPMtsaufUbxinxIJ8Qf-miOwsLiRMFNmPrC3ny9Y8YM-Pa0eDThmenY4z6r1u6v15YfV9Zf3Hy8vrldOgZxXpHppHCjgDTROglTCKMQWHSfQ0A9EyjVldnIA02gBhHwQUvJOSWzlWfVmLzst37fUOwpzwtFOyW8x_bIRvf33JvhbexN3FmTT8U4XgfODQIolhDzbrc-OxhEDxSVb4K2W2pgCNnvQpZhzouH4iOD2rg27sfs27F0bVoAtbZS1F38bvF86xF-AlwcAs8NxSBicz0cOOEjTaXH_Uypp7jwlm52n4Kj3idxs--j_7-Q3uxOpew</recordid><startdate>20080402</startdate><enddate>20080402</enddate><creator>Lam, Alicia F.</creator><creator>Krogh, Berit O.</creator><creator>Symington, Lorraine S.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7TM</scope><scope>M7N</scope><scope>5PM</scope></search><sort><creationdate>20080402</creationdate><title>Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair</title><author>Lam, Alicia F. ; Krogh, Berit O. ; Symington, Lorraine S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c523t-e5d37c2520424c3235175aa8ac0e262dfee5c40e2c3f274612ea0f1330953a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>Endodeoxyribonucleases - genetics</topic><topic>Endodeoxyribonucleases - metabolism</topic><topic>Exo1</topic><topic>Exodeoxyribonucleases - genetics</topic><topic>Exodeoxyribonucleases - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gamma Rays</topic><topic>Growth, nutrition, cell differenciation</topic><topic>Homologous recombination</topic><topic>Interstrand cross-links</topic><topic>Methyl Methanesulfonate - toxicity</topic><topic>Microbiology</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mre11</topic><topic>Mutagenesis. Repair</topic><topic>Mutagens - toxicity</topic><topic>Pso2</topic><topic>Radiation Tolerance - genetics</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - drug effects</topic><topic>Saccharomyces cerevisiae - enzymology</topic><topic>Saccharomyces cerevisiae - genetics</topic><topic>Saccharomyces cerevisiae - radiation effects</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lam, Alicia F.</creatorcontrib><creatorcontrib>Krogh, Berit O.</creatorcontrib><creatorcontrib>Symington, Lorraine S.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>DNA repair</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lam, Alicia F.</au><au>Krogh, Berit O.</au><au>Symington, Lorraine S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair</atitle><jtitle>DNA repair</jtitle><addtitle>DNA Repair (Amst)</addtitle><date>2008-04-02</date><risdate>2008</risdate><volume>7</volume><issue>4</issue><spage>655</spage><epage>662</epage><pages>655-662</pages><issn>1568-7864</issn><eissn>1568-7856</eissn><abstract>The Mre11 and Pso2 nucleases function in homologous recombination and interstrand cross-link (ICL) repair pathways, respectively, while the Exo1 nuclease is involved in homologous recombination and mismatch repair. Characterization of the sensitivity of single, double and triple mutants for these nucleases in
Saccharomyces cerevisiae to various DNA damaging agents reveals complex interactions that depend on the type of DNA damage. The
pso2 mutant is uniquely sensitive to agents that generate ICLs and
mre11-H125N shows the highest sensitivity of the single mutants for ionizing radiation and methyl methane sulfonate. However, elimination of all three nucleases confers higher sensitivity to IR than any of the single or double mutant combinations indicating a high degree of redundancy and versatility in the response to DNA damage. In response to ICL agents, double-strand breaks are still formed in the triple nuclease mutant indicating that none of these nucleases are responsible for unhooking cross-links.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>18295552</pmid><doi>10.1016/j.dnarep.2007.12.014</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Bacteriology Biological and medical sciences DNA Damage DNA Repair Endodeoxyribonucleases - genetics Endodeoxyribonucleases - metabolism Exo1 Exodeoxyribonucleases - genetics Exodeoxyribonucleases - metabolism Fundamental and applied biological sciences. Psychology Gamma Rays Growth, nutrition, cell differenciation Homologous recombination Interstrand cross-links Methyl Methanesulfonate - toxicity Microbiology Molecular and cellular biology Molecular genetics Mre11 Mutagenesis. Repair Mutagens - toxicity Pso2 Radiation Tolerance - genetics Saccharomyces cerevisiae Saccharomyces cerevisiae - drug effects Saccharomyces cerevisiae - enzymology Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - radiation effects Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism |
| title | Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair |
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