Author(s): Ungar L, Harari Y, Toren A, Kupiec M
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Abstract Telomeres are specialized DNA-protein structures at the ends of eukaryotic chromosomes. Telomeric DNA is synthesized by telomerase, which is expressed only at the early stages of development [1, 2]. To become malignant, any cell has to be able to replenish telomeres . Thus, understanding how telomere length is monitored has significant medical implications, especially in the fields of aging and cancer. In yeast, telomerase is constitutively active. A large network of genes participates in controlling telomere length [4-8]. Tor1 and Tor2 (targets of rapamycin ) are two similar kinases that regulate cell growth . Both can be found as part of the TOR complex 1 (TORC1 ), which coordinates the response to nutrient starvation and is sensitive to rapamycin . The rapamycin-insensitive TOR complex 2 (TORC2) contains only Tor2 and regulates actin cytoskeleton polarization . Here we provide evidence for a role of TORC1 in telomere shortening upon starvation in yeast cells. The TORC1 signal is transduced by the Gln3/Gat1/Ure2 pathway, which controls the levels of the Ku heterodimer, a telomere regulator. We discuss the potential implications for the usage of rapamycin as a therapeutic agent against cancer and the effect that calorie restriction may have on telomere length. Copyright © 2011 Elsevier Ltd. All rights reserved.
This article was published in Curr Biol
and referenced in Fungal Genomics & Biology