The mus206 gene of Drosophila melanogaster is required in the excision repair of alkylation-induced DNA lesions

Wen-Ya Huang, P. Dennis Smith

研究成果: Review article

2 引文 (Scopus)

摘要

The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.

原文English
頁(從 - 到)81-88
頁數8
期刊Mutation Research - DNA Repair
384
發行號2
DOIs
出版狀態Published - 1997 一月 1

指紋

Alkylation
Methyl Methanesulfonate
Drosophila melanogaster
DNA Repair
Repair
Genes
DNA
Mutation
Embryonic Structures
DNA Repair-Deficiency Disorders
Hatches
Primary Cell Culture
Cell culture
Drosophila
Larva
Nucleotides
Defects

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Toxicology
  • Genetics

引用此文

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title = "The mus206 gene of Drosophila melanogaster is required in the excision repair of alkylation-induced DNA lesions",
abstract = "The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.",
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T1 - The mus206 gene of Drosophila melanogaster is required in the excision repair of alkylation-induced DNA lesions

AU - Huang, Wen-Ya

AU - Smith, P. Dennis

PY - 1997/1/1

Y1 - 1997/1/1

N2 - The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.

AB - The mus206(A1) mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-54.8. Sex-linked recessive lethal mutation tests indicate that mus206(A1) exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206(A1) mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.

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