okra and spindle-B encode components of the RAD52 DNA repair pathway and affect meiosis and patterning in Drosophila oogenesis

  1. Amin Ghabrial2,
  2. Robert P. Ray1,2, and
  3. Trudi Schüpbach3
  1. Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544 USA

Abstract

okra (okr), spindle-B (spnB), andspindle-D (spnD) are three members of a group of female sterile loci that produce defects in oocyte and egg morphology, including variable dorsal–ventral defects in the eggshell and embryo, anterior–posterior defects in the follicle cell epithelium and in the oocyte, and abnormalities in oocyte nuclear morphology. Many of these phenotypes reflect defects in grk-Egfr signaling processes, and can be accounted for by a failure to accumulate wild-type levels of Gurken and Fs(1)K10. We have cloned okr and spnB, and show that okr encodes the Drosophila homolog of the yeast DNA-repair protein Rad54, and spnB encodes a Rad51-like protein related to the meiosis-specific DMC1 gene. In functional tests of their role in DNA repair, we find that okrbehaves like its yeast homolog in that it is required in both mitotic and meiotic cells. In contrast, spnB and spnD appear to be required only in meiosis. The fact that genes involved in meiotic DNA metabolism have specific effects on oocyte patterning implies that the progression of the meiotic cell cycle is coordinated with the regulation of certain developmental events during oogenesis.

Keywords

Footnotes

  • 1 Present address: Department of Molecular and Cellular Biology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912 USA.

  • 2 These authors contributed equally to this work.

  • 3 Corresponding author.

  • E-MAIL gschupbach{at}molbiol.princeton.edu; FAX (609) 258-1547.

    • Received May 1, 1998.
    • Accepted June 29, 1998.
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