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Vol. 12, No. 17, pp. 2711-2723, September 1, 1998
Howard Hughes Medical Institute, Department of Molecular Biology,
Princeton University, Princeton, New Jersey 08544 USA
okra (okr), spindle-B (spnB), and
spindle-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 okr
behaves 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.
[Key Words: okra; spindle-B; spindle-D; patterning; meiosis; Drosophila]
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