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Molecular and Cellular Biology, February 2009, p. 965-985, Vol. 29, No. 4
0270-7306/09/$08.00+0     doi:10.1128/MCB.00817-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification{triangledown} ,{dagger}

Nathalie Grandin and Michel Charbonneau*

UMR CNRS no. 5239, Ecole Normale Supérieure de Lyon, IFR128 BioSciences Gerland, 69364 Lyon, France

Received 21 May 2008/ Returned for modification 23 June 2008/ Accepted 21 November 2008

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, postsenescence 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- and 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 on the Rad51 recombinase and Rad59, thus making it distinct from both the type II (budding yeast ALT [alternative lengthening of telomeres]) and type I pathways amplifying the TG1-3 repeats and subtelomeric sequences, respectively. The ILT pathway also required the Rad1 endonuclease and Elg1, a replication factor C (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 repeat amplification are discussed. The effects of inherited long telomeres on Rad52-dependent recombination are also reported.

* Corresponding author. Mailing address: Ecole Normale Supérieure de Lyon, UMR CNRS 5239, 46, allée d'Italie, 69364 Lyon, France. Phone: (33) 47272 8170. Fax: (33) 47272 8080. E-mail: Michel.CHARBONNEAU{at}ens-lyon.fr

{triangledown} Published ahead of print on 1 December 2008.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, February 2009, p. 965-985, Vol. 29, No. 4
0270-7306/09/$08.00+0     doi:10.1128/MCB.00817-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Meznikova, M., Erdmann, N., Allsopp, R., Harrington, L. A. (2009). Telomerase reverse transcriptase-dependent telomere equilibration mitigates tissue dysfunction in mTert heterozygotes. DMM 2: 620-626 [Abstract] [Full Text]  
  • LeBel, C., Rosonina, E., Sealey, D. C. F., Pryde, F., Lydall, D., Maringele, L., Harrington, L. A. (2009). Telomere Maintenance and Survival in Saccharomyces cerevisiae in the Absence of Telomerase and RAD52. Genetics 182: 671-684 [Abstract] [Full Text]  


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