Abstract: In the absence of telomerase, telomeres erode, provoking accumulation of DNA damage and death by senescence. Rare survivors arise, however, due to Rad52-based amplification of telomeric sequences by homologous recombination. The present study reveals that, in budding yeast cells, post-senescence survival relying on amplification of the TG1-3 telomeric repeats can take place in the absence of Rad52 when overelongated telomeres are present during senescence (hence its designation ILT, for Inherited-Long-Telomere, pathway). By growth competition, the Rad52-independent pathway was almost as efficient as the Rad51-, Rad52-dependent pathway that predominates in telomerase-negative cells. The ILT pathway could also be triggered by increased telomerase accessibility before telomerase removal, combined with loss of telomere protection, indicating that prior accumulation of recombination proteins was not required. The ILT pathway was dependent on Rad50 and Mre11 but not the RAD51 recombinase and Rad59, thus making it distinct from both the type II (budding yeast ALT) and type I pathways amplifying the TG1-3 repeats and subtelomeric sequences, respectively. The ILT pathway also required the Rad1 endonuclease and Elg1, an RFC-like complex subunit, but not Rad24 or Ctf18 (two subunits of two other RFC-like complexes), the DNL4 ligase, Yku70 or Nej1. Possible mechanisms for this Rad52-independent pathway of telomeric repeats amplification are discussed. Effects of inherited long telomeres on Rad52-dependent recombination are also reported.