Abstract
In telomerase negative yeast cells, Rad52-dependent recombination is activated to maintain telomeres. This recombination-mediated telomere elongation usually involves two independent pathways, type I and type II, and leads to generation of type I and type II survivors. It remains elusive whether the recombination-mediated telomere elongation prefers to take place on shorter or longer telomeres. In this study, we exploited the de novo telomere addition system to examine the telomere recombination event in telomerase negative cells. We show that recombination preferentially occurs on shorter rather than longer telomeres in both pre-survivors and established type II survivors. In type II survivors, the short VII–L telomeres could invade either terminal TG1–3 sequence or short tracts of TG1–3 sequence in subtelomeric Y′-X and Y′-Y′ junction to initiate recombination. Unexpectedly, short VII–L telomere recombination still takes place in type II survivors lacking either Rad50 or Rad59, which are required for type II survivor generation in senescing telomerase-null cells. Our results support the notion that Rad50 and Rad59 are not essential for the maintenance of type II survivors once established.
Highlights
Telomeres are the physical ends of eukaryotic chromosomes, and consist of telomeric DNA of repetitive sequence and protein complexes
This observation indicated that telomere recombination is in action in the senescing telomerase-null cells, but not efficient enough to repair all the short telomeres to prevent the cells from entering crisis and senescence
Our results suggest that the short VII–L telomeres can initiate recombination by invading both TG1–3 tracts being internal to Y9 sequence (Fig. 3C) and the very terminal TG1–3 sequence of other telomeres (Fig. 3B)
Summary
Telomeres are the physical ends of eukaryotic chromosomes, and consist of telomeric DNA of repetitive sequence and protein complexes. Like most of the eukaryotes, budding yeast elongates its telomeric DNA through a specialized reverse-transcriptase, telomerase, which adds telomeric DNA sequences to the 39 G-overhang using its intrinsic RNA template [6,7]. Most of the telomerase-null senescing cells eventually die, while a very small portion of cells can overcome the crisis and remain viable. These cells are called ‘‘survivors’’, whose chromosome ends are lengthened by homologous recombination [14,15]. Approximately 15% of immortalized human tumor cells apply the ALT mechanism to maintain telomeres [18,19]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call