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Carcinogenesis Advance Access first published online on April 28, 2005
This version published online on April 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi107
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received January 24, 2005
Revised April 15, 2005
Accepted April 19, 2005

CARCINOGENESIS

Effectors of mammalian telomere dysfunction: a comparative transcriptome analysis using mouse models

Sonia Franco 1, Andrés Canela 1, Peter Klatt 1, and María A. Blasco 1*

1 Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Center (CNIO), Melchor Fernández Almagro, 3, 28029 Madrid, Spain

* To whom correspondence should be addressed.
María A. Blasco, E-mail: mblasco{at}cnio.es


  Abstract

Critical telomere shortening in the absence of telomerase in late generation Terc-/- mice (G3 Terc-/-) or loss of telomere capping due to abrogation of the DNA repair/telomere binding protein Ku86 (Ku86-/- mice) results in telomere dysfunction and organismal premature aging. Here, we report on genome-wide transcription in mouse G3 Terc-/-, Ku86-/- and G3 Terc-/-/Ku86-/- germ cells using high-density oligonucleotide microarrays. Although a few transcripts are modulated specifically in Ku86- or Terc-deficient cells, the observed transcriptional response is mainly inductive and qualitatively similar for all three genotypes, with highest transcriptional induction observed in double mutant G3 Terc-/-/Ku86-/- cells compared to either single mutant. Analysis of 92 known genes induced in G3 Terc-/-/Ku86-/- germ cells compared to wild-type cells shows predominance of genes involved in cell adhesion, cell-to-cell and cell-to-matrix communication, as well as increased metabolic turnover and augmented antioxidant responses. In addition, the data presented in this study support the view that telomere dysfunction induces a robust compensatory response to rescue impaired germ cell function through the induction of survival signals related to the PI3-kinase pathway, as well as by the coordinated up-regulation of transcripts that are essential for mammalian spermatogenesis.

The originally published version of this paper was incorrect. The figures were missing and have now been included.
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