Mec1p associates with functionally compromised telomeres |
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| Authors: | Ronald E Hector Alo Ray Bo-Ruei Chen Rebecca Shtofman Kathleen L Berkner Kurt W Runge |
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| Institution: | (1) Department of Molecular Genetics, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Lerner Research Institute, 9500 Euclid Avenue, NE20, Cleveland, OH 44195, USA;(2) Department of Molecular Cardiology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Lerner Research Institute, 9500 Euclid Avenue, NB50, Cleveland, OH 44195, USA;(3) Department of Genetics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4920, USA;(4) Present address: NCAUR, ARS, USDA, 1815 N. University St., Peoria, IL 61604, USA;(5) Present address: Division of Radiology, 730 Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH 43210, USA; |
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| Abstract: | In many organisms, telomere DNA consists of simple sequence repeat tracts that are required to protect the chromosome end.
In the yeast Saccharomyces cerevisiae, tract maintenance requires two checkpoint kinases of the ATM family, Tel1p and Mec1p. Previous work has shown that Tel1p
is recruited to functional telomeres with shorter repeat tracts to promote telomerase-mediated repeat addition, but the role
of Mec1p is unknown. We found that Mec1p telomere association was detected as cells senesced when telomere function was compromised
by extreme shortening due to either the loss of telomerase or the double-strand break binding protein Ku. Exonuclease I effects
the removal of the 5' telomeric strand, and eliminating it prevented both senescence and Mec1p telomere association. Thus,
in contrast to Tel1p, Mec1p associates with short, functionally compromised telomeres. |
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