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Title: [Studies of the repair of radiation-induced genetic damage in Drosophila]. Annual progress report, July 1, 1991--June 1, 1992

Abstract

The primary goal of this program is to achieve a more thorough understanding of the mechanisms employed by higher organisms to resist DNA damage. Concurrently this effort contributes to an improved understanding of the processes of mutagenesis and carcinogenesis in higher eukaryotes. Drosophila was initially chosen as a model organism for investigating functions that control mutagen resistance because of the ease with which one can isolate and characterize mutagen-sensitive mutants in this multicellular organism. This laboratory then went on to investigate the DNA repair defects of such mutants while others performed complementary genetic and cytogenetic studies which relate DNA repair processes to mutagenesis and chromosome stability. Currently, recombinant DNA technology is being employed to investigate the mechanisms of mutagen resistance defined by those mutants. The following two studies experienced the most significant progress during the past year: cloning and genetic characterization of the mus209 gene, and genetic and molecular analysis of the mus308 gene.

Publication Date:
Research Org.:
Univ. of California, Davis, CA (United States)
Sponsoring Org.:
USDOE Office of Energy Research, Washington, DC (United States)
OSTI Identifier:
663538
Report Number(s):
DOE/ER/60538-T5
ON: DE98007384; BR: HA0202020;KP0402000; TRN: AHC29818%%375
DOE Contract Number:
FG03-87ER60538
Resource Type:
Technical Report
Resource Relation:
Other Information: PBD: [1992]
Country of Publication:
United States
Language:
English
Subject:
56 BIOLOGY AND MEDICINE, APPLIED STUDIES; PROGRESS REPORT; STRAND BREAKS; DNA REPAIR; MUTAGENESIS; DROSOPHILA; DNA-CLONING; GENES; CARCINOGENESIS; RECOMBINANT DNA

Citation Formats

NONE. [Studies of the repair of radiation-induced genetic damage in Drosophila]. Annual progress report, July 1, 1991--June 1, 1992. United States: N. p., 1992. Web. doi:10.2172/663538.
NONE. [Studies of the repair of radiation-induced genetic damage in Drosophila]. Annual progress report, July 1, 1991--June 1, 1992. United States. doi:10.2172/663538.
NONE. Thu . "[Studies of the repair of radiation-induced genetic damage in Drosophila]. Annual progress report, July 1, 1991--June 1, 1992". United States. doi:10.2172/663538. https://www.osti.gov/servlets/purl/663538.
@article{osti_663538,
title = {[Studies of the repair of radiation-induced genetic damage in Drosophila]. Annual progress report, July 1, 1991--June 1, 1992},
author = {NONE},
abstractNote = {The primary goal of this program is to achieve a more thorough understanding of the mechanisms employed by higher organisms to resist DNA damage. Concurrently this effort contributes to an improved understanding of the processes of mutagenesis and carcinogenesis in higher eukaryotes. Drosophila was initially chosen as a model organism for investigating functions that control mutagen resistance because of the ease with which one can isolate and characterize mutagen-sensitive mutants in this multicellular organism. This laboratory then went on to investigate the DNA repair defects of such mutants while others performed complementary genetic and cytogenetic studies which relate DNA repair processes to mutagenesis and chromosome stability. Currently, recombinant DNA technology is being employed to investigate the mechanisms of mutagen resistance defined by those mutants. The following two studies experienced the most significant progress during the past year: cloning and genetic characterization of the mus209 gene, and genetic and molecular analysis of the mus308 gene.},
doi = {10.2172/663538},
journal = {},
number = ,
volume = ,
place = {United States},
year = {Thu Dec 31 00:00:00 EST 1992},
month = {Thu Dec 31 00:00:00 EST 1992}
}

Technical Report:

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  • The most interesting discovery made over the past year derives from sequence analysis of cDNAs from the putative mus308 gene. The theoretical translation product of this gene contains a DNA polymerase domain near the carboxy terminus and DNA/RNA helicase motifs near the amino terminus. There is currently no precedent in the literature for a single polypeptide containing both of these domains. The protein appears to be a novel DNA repair enzyme which should be fruitful ground for future enzymological analysis. The authors have identified two ORFs by sequence analysis of the transforming fragment containing the mei-41 gene and of correspondingmore » cDNAs. ORF 1 includes the P element insertion sites and encodes a peptide of 757 amino acids. ORF 2 starts 900 base pairs downstream of ORF 1 and encodes a peptide of 1,037 amino acids. This putative peptide shows homology to the yeast DNA repair genes, rad50 of S. cerevisiae and rad3 of S. pombe.« less
  • Research is focused on the following areas: characterization of DNA double-strand break repair; using injected oligonucleotides as templates to repair double-strand DNA breaks; analysis of a gene required for postreplication repair; cloning of a gene required for resistance to DNA cross-linking agents; cloning of a gene required for excision repair; cloning of a gene required for X-ray resistance; and transposon tagging DNA repair genes.
  • At this time last year, we had identified two genes in Drosophila that are required for repair of double strand breaks. These genes (mei-41 and mus302) have now been completely analyzed. We have developed an efficient system for site-directed mutagenesis using injected oligonucleotides as a template for the repair of double strand breaks. mus308, a gene responsible for resistance to DNA cross-linking, is being recovered through chromosome walking. It is believed this gene may be the Drosophila analog of the human Fanconi anemia A gene. A collaborative effort to clone the excision repair gene, mei-9, is under way. The X-raymore » resistance gene mus209 has been cloned. Finally, we are analyzing a group of mus mutations from other labs which we have tagged with a single transposon inserted randomly into one of the two major autosomes. 4 refs.« less
  • Research progress is reported in the following areas: (1) characterization of a photo-repair deficient mutant in Drosophila; (2) the role of poly(ADPR)polymerase in Drosophila repair; and (3) service functions. (ACR)
  • The primary goal of this study is to achieve a more thorough understanding of the mechanisms employed by higher organisms to repair DNA damage induced by both ionizing and nonionizing radiation. These studies are also contributing to an improved understanding of the processes of mutagenesis and carcinogenesis in higher eukaryotes. The studies employ Drosophila as a model organism for investigating repair functions that are common to all higher eukaryotes. Drosophila was chosen in the early phases of this study primarily because of the ease with which one can isolate and characterize repair-deficient mutants in a metazoan organism. The laboratory hasmore » gone on to investigate the metabolic defects of such mutants while others have performed complementary genetic and cytogenetic studies which relate DNA repair processes to mutagenesis and chromosome stability. The repair studies have exploited the capacity to introduce mutant Drosophila cells into tissue culture and thereby compare repair defects directly with those of homologous human disorders. Researchers are currently employing recombinant DNA technology to investigate the mechanisms of the DNA repair pathways defined by those mutants.« less