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Vol. 12, Issue 7, 2023-2030, July 2001
and
*Department of Molecular Biology and Genetics and Graduate Program
in Human Genetics, Johns Hopkins University School of Medicine,
Baltimore, Maryland 21205; and Telomere dysfunction results in fertility defects in a number of
organisms. Although data from fission yeast and Caenorhabditis elegans suggests that telomere dysfunction manifests itself
primarily as defects in proper meiotic chromosome segregation, it is
unclear how mammalian telomere dysfunction results in germ cell death. To investigate the specific effects of telomere dysfunction on mammalian germ cell development, we examined the meiotic progression and germ cell apoptosis in late generation telomerase null mice. Our
results indicate that chromosome asynapsis and missegregation are not
the cause of infertility in mice with shortened telomeres. Rather,
telomere dysfunction is recognized at the onset of meiosis, and cells
with telomeric defects are removed from the germ cell precursor pool.
This germ cell telomere surveillance may be an important mechanism to
protect against the transmission of dysfunctional telomeres and
chromosomal abnormalities.
Dana Farber Cancer
Institute and Harvard Medical School, Boston, Massachusetts 02115
Corresponding author. E-mail address:
cgreider{at}jhmi.edu.
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