Telomerase-independent lengthening of yeast telomeres occurs by an abrupt Rad50p-dependent, Rif-inhibited recombinational process

Mol Cell. 2000 Oct;6(4):947-52. doi: 10.1016/s1097-2765(05)00094-8.


Type II survivors arise in Saccharomyces cells lacking telomerase by a recombinational pathway that results in very long and heterogeneous length telomeres. Here we show that type II telomeres appeared abruptly in a population of cells with very short telomeres. Once established, these long telomeres progressively shortened. Short telomeres were substrates for rare, one-step lengthening events. The generation of type II survivors was absolutely Rad50p dependent. In a telomerase-proficient cell, the telomere-binding Rif proteins inhibited telomerase lengthening of telomeres. In a telomerase-deficient strain, Rif proteins, especially Rif2p, inhibited type II recombination. These data argue that only short telomeres are substrates for type II recombination and suggest that the donor for this recombination is not a chromosomal telomere.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Carrier Proteins / metabolism*
  • DNA-Binding Proteins*
  • Fungal Proteins / metabolism*
  • Recombination, Genetic*
  • Saccharomyces cerevisiae / genetics*
  • Saccharomyces cerevisiae Proteins*
  • Telomerase / metabolism
  • Telomere / physiology*
  • Telomere / ultrastructure
  • Telomere-Binding Proteins
  • Zinc Fingers


  • Carrier Proteins
  • DNA-Binding Proteins
  • Fungal Proteins
  • RAD50 protein, S cerevisiae
  • RIF2 protein, S cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Telomere-Binding Proteins
  • Telomerase