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Vol. 15, No. 5, pp. 522-534, March 1, 2001
Departments of Developmental Biology and Genetics, Stanford
University School of Medicine, Stanford, California 94305-5329, USA
We investigated the roles of Caenorhabditis elegans MRE-11
in multiple cellular processes required to maintain genome integrity. Although yeast Mre11 is known to promote genome stability through several diverse pathways, inviability of vertebrate cells that lack
Mre11 has hindered elucidation of the in vivo roles of this conserved
protein in metazoan biology. Worms homozygous for an mre-11
null mutation are viable, allowing us to demonstrate in vivo
requirements for MRE-11 in meiotic recombination and DNA repair. In
mre-11 mutants, meiotic crossovers are not detected, and oocyte
chromosomes lack chiasmata but appear otherwise intact. 
-irradiation
of mre-11 mutant germ cells during meiotic prophase eliminates
progeny survivorship and induces chromosome fragmentation and other
cytologically visible abnormalities, indicating a defect in repair of
radiation-induced chromosome damage. Whereas mre-11 mutant germ
cells are repair-deficient, they retain function of the meiotic
G2 DNA damage checkpoint that triggers germ cell apoptosis in
response to ionizing radiation. Although mre-11/mre-11 animals derived from heterozygous parents are viable and produce many embryos,
there is a marked drop both in the number and survivorship of embryos
produced by succeeding generations. This progressive loss of fecundity
and viability indicates that MRE-11 performs a function essential for
maintaining reproductive capacity in the species.
[Key Words: Meiosis; recombination; DNA repair; checkpoint; C. elegans; Mre11; mre-11]
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