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Tel1 kinase and subtelomere‐bound Tbf1 mediate preferential elongation of short telomeres by telomerase in yeast
Author(s) -
Arnerić Milica,
Lingner Joachim
Publication year - 2007
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7401082
Subject(s) - telomere , subtelomere , telomerase , telomere binding protein , biology , microbiology and biotechnology , elongation factor , elongation , mutation , genetics , dna , gene , dna binding protein , transcription factor , rna , ribosome , materials science , ultimate tensile strength , metallurgy
Telomerase enables telomere length homeostasis, exhibiting increasing preference for telomeres as their lengths decline. This regulation involves telomere repeat‐bound Rap1, which provides a length‐dependent negative feedback mechanism, and the Tel1 and Mec1 kinases, which are positive regulators of telomere length. By analysing telomere elongation of wild‐type chromosome ends at single‐molecule resolution, we show that in tel1 Δ cells the overall frequency of elongation decreases considerably, explaining their short telomere phenotype. At an artificial telomere lacking a subtelomeric region, telomere elongation no longer increases with telomere shortening in tel1 Δ cells. By contrast, a natural telomere, containing subtelomeric sequence, retains a preference for the elongation of short telomeres. Tethering of the subtelomere binding protein Tbf1 to the artificial telomere in tel1 Δ cells restored preferential telomerase action at short telomeres; thus, Tbf1 might function in parallel to Tel1, which has a crucial role in a TG‐repeat‐controlled pathway for the activation of telomerase at short telomeres.