Greider Carol W
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.
Genes Dev. 2016 Jul 1;30(13):1483-91. doi: 10.1101/gad.280578.116.
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.
端粒长度围绕一个平衡设定点进行调节。端粒在复制过程中缩短，并由端粒酶延长。长度平衡的破坏会导致疾病；因此，了解在分子水平上调节长度的机制很重要。目前关于调节端粒酶接近端粒以使其延长的蛋白质计数模型，无法解释越来越多关于DNA复制在端粒长度调节中作用的证据。在此，我提出一种替代模型：复制叉模型，它可以解释复制叉的通过以及起始点激发的调节如何影响端粒长度。
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