1998
DOI: 10.1007/s004120050335
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Inhibition of the M r 70,000 S6 kinase pathway by rapamycin results in chromosome malsegregation in yeast and mammalian cells

Abstract: The antifungal and immunosuppressive drug rapamycin arrests the cell cycle in G1-phase in both yeast and mammalian cells. In mammalian cells, rapamycin selectively inhibits phosphorylation and activation of p70 S6 kinase (p70(S6K)), a protein involved in the translation of a subset of mRNAs, without affecting other known kinases. We now report that rapamycin causes chromosome malsegregation in mammalian and yeast cells. Chromosome malsegregation was determined by metaphase chromosome analysis of human lymphocy… Show more

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Cited by 17 publications
(18 citation statements)
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“…We show that mTOR becomes also activated post NEBD in the human oocyte, with strong signal at midbody in the MII oocyte, suggesting its similar role in the human oocyte meiosis in specific translational regulation, as it plays in the mouse oocyte. Here, mTOR pathway might contribute to the age related chromosome segregation errors in the woman oocytes, similarly as it has been documented in the mouse model, 9 as well as in mammalian and yeast cells 71 . Lapasset et al 7 .…”
Section: Resultssupporting
confidence: 53%
“…We show that mTOR becomes also activated post NEBD in the human oocyte, with strong signal at midbody in the MII oocyte, suggesting its similar role in the human oocyte meiosis in specific translational regulation, as it plays in the mouse oocyte. Here, mTOR pathway might contribute to the age related chromosome segregation errors in the woman oocytes, similarly as it has been documented in the mouse model, 9 as well as in mammalian and yeast cells 71 . Lapasset et al 7 .…”
Section: Resultssupporting
confidence: 53%
“…Anaphase bridges have been shown to arise from several defined mechanisms, most often involving a lack of proper telomere maintenance [38] sometimes involving topoisomerase function [45] or, helicase [46] function. Two publications from the same group offer evidence that RAP treatment can lead to chromosomal non-disjunction during M-phase in yeast and mammalian cell cultures [47], [48]. Strikingly, estradiol treatment consistently decreased anaphase bridges in mitotic SIGC versus cells treated with the corresponding concentration of RAP alone.…”
Section: Discussionmentioning
confidence: 99%
“…Rapamycin treatment rapidly causes microtubule instability and defects in microtubulerelated functions, such as spindle elongation and orientation, chromosomal segregation, nuclear migration, and karyogamy (44). Rapamycin treatment also leads to chromosomal missegregation in both mammalian cells and yeast (44,45). Chromosomal instability (CIN) is an important contributing factor to human cancer (reviewed in ref.…”
Section: Resultsmentioning
confidence: 99%