Regulating telomere length from the inside out: the replication fork model
- Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA;
- Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA
- Corresponding author: cgreider{at}jhmi.edu
Abstract
Telomere length is regulated around an equilibrium set point. Telomeres shorten during replication and are lengthened by telomerase. Disruption of the length equilibrium leads to disease; thus, it is important to understand the mechanisms that regulate length at the molecular level. The prevailing protein-counting model for regulating telomerase access to elongate the telomere does not explain accumulating evidence of a role of DNA replication in telomere length regulation. Here I present an alternative model: the replication fork model that can explain how passage of a replication fork and regulation of origin firing affect telomere length.
Keywords
Footnotes
-
Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.280578.116.
-
Freely available online through the Genes & Development Open Access option.
This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.
