The chromosome ends of Saccharomyces cerevisiae
- 1 December 1995
- Vol. 11 (16) , 1553-1573
- https://doi.org/10.1002/yea.320111604
Abstract
Yeast chromosome ends are similar in structure and function to chromosome ends in most, if not all, eukaryotic organisms. There is a G‐rich terminal repeat at the ends which is maintained by telomerase. In addition to the classical functions of protecting the end from degradation and end‐to‐end fusions, and completing replication, yeast telomeres have several interesting properties including: non‐nucleosomal chromatin structure; transcriptional position effect variegation for genes with adjacent telomeres; nuclear peripheral localization; apparent physical clustering; non‐random recombinational interactions. A number of genes have been identified that are involved in modifying one or more of these properties. These include genes involved in general DNA metabolism, chromatin structure and telomere maintenance. Adjacent to the terminal repeat is a mosaic of middle repetitive elements that exhibit a great deal of polymorphism both between individual strains and among different chromosome ends. Much of the sequence redundancy in the yeast genome is found in the sub‐telomeric regions (within the last 25 kb of each end). The sub‐telomeric regions are generally low in gene density, low in transcription, low in recombination, and they are late replicating. The only element which appears to be shared by all chromosome ends is part of the previously defined X element containing an ARS consensus. Most of the ‘core’ X elements also contain an Abf1p binding site and a URS1‐like element, which may have consequences for the chromatin structure, nuclear architecture and transcription of native telomeres. Possible functions of sub‐telomeric repeats include: fillers for increasing chromosome size to some minimum threshold level necessary for chromosome stability; barrier against transcriptional silencing; a suitable region for adaptive amplification of genes; secondary mechanism of telomere maintenance via recombination when telomerase activity is absent.Keywords
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