Document Type
Article
Publication Date
1-1-1996
Publication Title
Genes and Development
Abstract
One of the central requirements for eukaryotic chromosome stability is the maintenance of the simple sequence tracts at telomeres. In this study, we use genetic and physical assays to reveal the nature of a novel mechanism by which telomere length is controlled. This mechanism, telomeric rapid deletion (TRD), is capable of reducing elongated telomeres to wild-type tract length in an apparently single-division process. The deletion of telomeres to wild- type lengths is stimulated by the hpr1 mutation, suggesting that TRD in these cells is the consequence of an intrachromatid pathway. Paradoxically, TRD is also dependent on the lengths of the majority of nonhomologous telomeres in the cell. Defects in the chromatin-organizing protein Sir3p increase the rate of hpr1-induced rapid deletion and specifically change the spectrum of rapid deletion events. We propose a model in which interactions among telosomes of nonhomologous chromosomes form higher order complexes that restrict the access of the intrachromatid recombination machinery to telomeres. This mechanism of size control is distinct from that mediated through telomerase and is likely to maintain telomere length within a narrow distribution.
DOI
10.1101/gad.10.11.1310
Version
Publisher's PDF
Recommended Citation
Li, Bibo and Lustig, Arthur J., "A Novel Mechanism for Telomere Size Control in Saccharomyces cerevisiae" (1996). Biological, Geological, and Environmental Faculty Publications. 224.
https://engagedscholarship.csuohio.edu/scibges_facpub/224
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
Volume
10
Issue
11
