Identification of a second locus in Drosophila melanogaster required for excision repair
The mus(2)201 locus in Drosophila is defined by two mutant alleles that render homozygous larvae hypersensitive to mutagens. Both alleles confer strong in vivo somatic sensitivity to treatment by methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity to X-...
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| Veröffentlicht in: | Genetics (Austin) 1982-02, Vol.100 (2), p.239-257 |
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| container_title | Genetics (Austin) |
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| creator | Boyd, J.B Snyder, R.D Harris, P.V Presley, J.M Boyd, S.F Smith, P.D |
| description | The mus(2)201 locus in Drosophila is defined by two mutant alleles that render homozygous larvae hypersensitive to mutagens. Both alleles confer strong in vivo somatic sensitivity to treatment by methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity to X-irradiation. Unlike the excision-defective mei-9 mutants identified in previous studies, the mus(2)201 mutants do not affect female fertility and do not appear to influence recombination proficiency or chromosome segregation in female meiocytes.--Three independent biochemical assays reveal that cell cultures derived from embryos homozygous for the mus(2)D1 allele are devoid of detectable excision repair. 1. Such cells quantitatively retain pyrimidine dimers in their DNA for 24 hr following UV exposure. 2. No measurable unscheduled DNA synthesis is induced in mutant cultures by UV treatment. 3. Single-strand DNA breaks, which are associated with normal excision repair after treatment with either UV or N-acetoxy-N-acetyl-2-aminofluorene, are much reduced in these cultures. Mutant cells possess a normal capacity for postreplication repair and the repair of single-strand breaks induced by X-rays. |
| doi_str_mv | 10.1093/genetics/100.2.239 |
| format | Article |
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Both alleles confer strong in vivo somatic sensitivity to treatment by methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity to X-irradiation. Unlike the excision-defective mei-9 mutants identified in previous studies, the mus(2)201 mutants do not affect female fertility and do not appear to influence recombination proficiency or chromosome segregation in female meiocytes.--Three independent biochemical assays reveal that cell cultures derived from embryos homozygous for the mus(2)D1 allele are devoid of detectable excision repair. 1. Such cells quantitatively retain pyrimidine dimers in their DNA for 24 hr following UV exposure. 2. No measurable unscheduled DNA synthesis is induced in mutant cultures by UV treatment. 3. Single-strand DNA breaks, which are associated with normal excision repair after treatment with either UV or N-acetoxy-N-acetyl-2-aminofluorene, are much reduced in these cultures. Mutant cells possess a normal capacity for postreplication repair and the repair of single-strand breaks induced by X-rays.</description><identifier>ISSN: 0016-6731</identifier><identifier>ISSN: 1943-2631</identifier><identifier>EISSN: 1943-2631</identifier><identifier>DOI: 10.1093/genetics/100.2.239</identifier><identifier>PMID: 6809529</identifier><language>eng</language><publisher>United States: Genetics Soc America</publisher><subject>Alleles ; animal breeding ; animal genetics ; Animals ; arthropods ; Crosses, Genetic ; DNA Repair ; DNA Replication ; Drosophila melanogaster ; Drosophila melanogaster - drug effects ; Drosophila melanogaster - genetics ; Drosophila melanogaster - radiation effects ; entomology ; Female ; Genetic Complementation Test ; Homozygote ; Investigations ; Larva - drug effects ; Larva - radiation effects ; Male ; Meiosis ; Mutagens - pharmacology ; Mutation ; Reproduction ; Ultraviolet Rays</subject><ispartof>Genetics (Austin), 1982-02, Vol.100 (2), p.239-257</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c549t-7b3be929bc73b79d416aada9832cc7bcaccf93962f5b7036d813269475fcefc53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6809529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boyd, J.B</creatorcontrib><creatorcontrib>Snyder, R.D</creatorcontrib><creatorcontrib>Harris, P.V</creatorcontrib><creatorcontrib>Presley, J.M</creatorcontrib><creatorcontrib>Boyd, S.F</creatorcontrib><creatorcontrib>Smith, P.D</creatorcontrib><title>Identification of a second locus in Drosophila melanogaster required for excision repair</title><title>Genetics (Austin)</title><addtitle>Genetics</addtitle><description>The mus(2)201 locus in Drosophila is defined by two mutant alleles that render homozygous larvae hypersensitive to mutagens. Both alleles confer strong in vivo somatic sensitivity to treatment by methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity to X-irradiation. Unlike the excision-defective mei-9 mutants identified in previous studies, the mus(2)201 mutants do not affect female fertility and do not appear to influence recombination proficiency or chromosome segregation in female meiocytes.--Three independent biochemical assays reveal that cell cultures derived from embryos homozygous for the mus(2)D1 allele are devoid of detectable excision repair. 1. Such cells quantitatively retain pyrimidine dimers in their DNA for 24 hr following UV exposure. 2. No measurable unscheduled DNA synthesis is induced in mutant cultures by UV treatment. 3. Single-strand DNA breaks, which are associated with normal excision repair after treatment with either UV or N-acetoxy-N-acetyl-2-aminofluorene, are much reduced in these cultures. Mutant cells possess a normal capacity for postreplication repair and the repair of single-strand breaks induced by X-rays.</description><subject>Alleles</subject><subject>animal breeding</subject><subject>animal genetics</subject><subject>Animals</subject><subject>arthropods</subject><subject>Crosses, Genetic</subject><subject>DNA Repair</subject><subject>DNA Replication</subject><subject>Drosophila melanogaster</subject><subject>Drosophila melanogaster - drug effects</subject><subject>Drosophila melanogaster - genetics</subject><subject>Drosophila melanogaster - radiation effects</subject><subject>entomology</subject><subject>Female</subject><subject>Genetic Complementation Test</subject><subject>Homozygote</subject><subject>Investigations</subject><subject>Larva - drug effects</subject><subject>Larva - radiation effects</subject><subject>Male</subject><subject>Meiosis</subject><subject>Mutagens - pharmacology</subject><subject>Mutation</subject><subject>Reproduction</subject><subject>Ultraviolet Rays</subject><issn>0016-6731</issn><issn>1943-2631</issn><issn>1943-2631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1982</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUtv1DAUhS1UVIbCH6iE6hW7TP1InHhTqRpelSqxgErsrBvnOuMqiad2wsC_x9UMpawsy-d-1-ccQs45W3Om5WWPE87epkvO2FqshdQvyIrrUhZCSX5CVoxxVaha8lfkdUr3jDGlq-aUnKqG6UroFflx0-E0e-ctzD5MNDgKNKENU0eHYJdE_UQ_xJDCbusHoCMOMIUe0oyRRnxYfMSOuhAp_rI-PSIi7sDHN-SlgyHh2-N5Ru4-ffy--VLcfv18s7m-LWxV6rmoW9miFrq1tWxr3ZVcAXSgGymsrVsL1jottRKuamsmVddwKZQu68pZdLaSZ-TqwN0t7YidzW4iDGYX_Qjxtwngzf8vk9-aPvw0XDCeU8iA90dADA8LptmMPlkcsk8MSzK8KnnJ6jILxUFocxwpontawpl57MP87SPfmBEm95GH3j3_3tPIsYB_27e-3-5zmCaNMAxZzc1-v38OujgIHQQDffTJ3H3LFiTjuhGl0vIPUyeiUw</recordid><startdate>19820201</startdate><enddate>19820201</enddate><creator>Boyd, J.B</creator><creator>Snyder, R.D</creator><creator>Harris, P.V</creator><creator>Presley, J.M</creator><creator>Boyd, S.F</creator><creator>Smith, P.D</creator><general>Genetics Soc America</general><scope>FBQ</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>7SS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>19820201</creationdate><title>Identification of a second locus in Drosophila melanogaster required for excision repair</title><author>Boyd, J.B ; Snyder, R.D ; Harris, P.V ; Presley, J.M ; Boyd, S.F ; Smith, P.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c549t-7b3be929bc73b79d416aada9832cc7bcaccf93962f5b7036d813269475fcefc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1982</creationdate><topic>Alleles</topic><topic>animal breeding</topic><topic>animal genetics</topic><topic>Animals</topic><topic>arthropods</topic><topic>Crosses, Genetic</topic><topic>DNA Repair</topic><topic>DNA Replication</topic><topic>Drosophila melanogaster</topic><topic>Drosophila melanogaster - drug effects</topic><topic>Drosophila melanogaster - genetics</topic><topic>Drosophila melanogaster - radiation effects</topic><topic>entomology</topic><topic>Female</topic><topic>Genetic Complementation Test</topic><topic>Homozygote</topic><topic>Investigations</topic><topic>Larva - drug effects</topic><topic>Larva - radiation effects</topic><topic>Male</topic><topic>Meiosis</topic><topic>Mutagens - pharmacology</topic><topic>Mutation</topic><topic>Reproduction</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boyd, J.B</creatorcontrib><creatorcontrib>Snyder, R.D</creatorcontrib><creatorcontrib>Harris, P.V</creatorcontrib><creatorcontrib>Presley, J.M</creatorcontrib><creatorcontrib>Boyd, S.F</creatorcontrib><creatorcontrib>Smith, P.D</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genetics (Austin)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boyd, J.B</au><au>Snyder, R.D</au><au>Harris, P.V</au><au>Presley, J.M</au><au>Boyd, S.F</au><au>Smith, P.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of a second locus in Drosophila melanogaster required for excision repair</atitle><jtitle>Genetics (Austin)</jtitle><addtitle>Genetics</addtitle><date>1982-02-01</date><risdate>1982</risdate><volume>100</volume><issue>2</issue><spage>239</spage><epage>257</epage><pages>239-257</pages><issn>0016-6731</issn><issn>1943-2631</issn><eissn>1943-2631</eissn><abstract>The mus(2)201 locus in Drosophila is defined by two mutant alleles that render homozygous larvae hypersensitive to mutagens. Both alleles confer strong in vivo somatic sensitivity to treatment by methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity to X-irradiation. Unlike the excision-defective mei-9 mutants identified in previous studies, the mus(2)201 mutants do not affect female fertility and do not appear to influence recombination proficiency or chromosome segregation in female meiocytes.--Three independent biochemical assays reveal that cell cultures derived from embryos homozygous for the mus(2)D1 allele are devoid of detectable excision repair. 1. Such cells quantitatively retain pyrimidine dimers in their DNA for 24 hr following UV exposure. 2. No measurable unscheduled DNA synthesis is induced in mutant cultures by UV treatment. 3. Single-strand DNA breaks, which are associated with normal excision repair after treatment with either UV or N-acetoxy-N-acetyl-2-aminofluorene, are much reduced in these cultures. Mutant cells possess a normal capacity for postreplication repair and the repair of single-strand breaks induced by X-rays.</abstract><cop>United States</cop><pub>Genetics Soc America</pub><pmid>6809529</pmid><doi>10.1093/genetics/100.2.239</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Genetics (Austin), 1982-02, Vol.100 (2), p.239-257 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Alleles animal breeding animal genetics Animals arthropods Crosses, Genetic DNA Repair DNA Replication Drosophila melanogaster Drosophila melanogaster - drug effects Drosophila melanogaster - genetics Drosophila melanogaster - radiation effects entomology Female Genetic Complementation Test Homozygote Investigations Larva - drug effects Larva - radiation effects Male Meiosis Mutagens - pharmacology Mutation Reproduction Ultraviolet Rays |
| title | Identification of a second locus in Drosophila melanogaster required for excision repair |
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