Biochemical Characterization of Repair-Deficient Mutants of Drosophila

  • James B. Boyd
  • Paul V. Harris
  • Christopher J. Osgood
  • Karen E. Smith
Part of the Basic Life Sciences book series (BLSC, volume 15)


DNA metabolism is being analyzed in cell cultures derived from the available mutagen-sensitive stocks. Thus far, mutants occurring at eleven different genetic loci in Drosophila melanogaster have been shown to be defective in DNA synthesis or repair. Mutants associated with the following genetic loci exhibit defects in the corresponding metabolic functions:
  • Excision Repair — mei-9, mus (2)201, mus (2)205, mus(3)308

  • Postreplication Repair — mei-41, mus(1)101, mus(1)104, mus (2)205, mus (3)302, mus (3)310, mus (3)311

  • DNA Synthesis — mus(1)101, mus(1)104, mus (2)205, mus (3)307, mus (3)308

The pleiotropic effect of several of these mutants indicates that their wild type alleles normally participate in more than one of these processes. Since mutants in at least three of these classes [mei-9, mei-41, mus(1)101] also alter meiotic recombination, their biochemical analysis in the more plentiful somatic cells can potentially reveal the function of the normal alleles in the rare meiotic tissues. A survey of the mutant properties is presented in Table 3.

The existence of a photorepair system has been documented in Drosophila, although no genetic blocks in that process have been identified. Identification of an AP-endonuclease activity suggests that Drosophila may possess a base excision mechanism. A technical advance is also described which will permit biochemical analysis of stocks in which homozygous females are sterile.


Excision Repair Meiotic Recombination Pyrimidine Dimer Homozygous Female Brain Ganglion 
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Copyright information

© Plenum Press, New York 1980

Authors and Affiliations

  • James B. Boyd
    • 1
  • Paul V. Harris
    • 1
  • Christopher J. Osgood
    • 1
  • Karen E. Smith
    • 1
  1. 1.Department of GeneticsUniversity of CaliforniaDavisUSA

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