Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

Ruben D. Ramirez, Carmela P. Morales, Brittney Shea Herbert, Jeffrey M. Rohde, Christina Passons, Jerry W. Shay, Woodring E. Wright

Research output: Contribution to journalArticle

380 Scopus citations

Abstract

Telomere shortening is the mechanism underlying replicative aging in fibroblasts. A variety of reports now claim that inactivation of the p161NK4a/pRB pathway is required in addition to telomere maintenance for the immortalization of cells such as skin keratinocytes and breast epithelial cells. We here show that the premature growth arrest of these cell types can be explained by an inadequate culture environment. Providing mesenchymal/epithelial interactions by cultivating the telomerase-expressing cells on feeder layers avoids the growth arrest associated with increased p161NK4a. These results do not support a telomere-independent mechanism of replicative aging.

Original languageEnglish (US)
Pages (from-to)398-403
Number of pages6
JournalGenes and Development
Volume15
Issue number4
DOIs
StatePublished - Mar 14 2001
Externally publishedYes

Keywords

  • Aging
  • Cancer
  • Cellular senescence
  • P16
  • Replicative aging
  • Telomeres

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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  • Cite this

    Ramirez, R. D., Morales, C. P., Herbert, B. S., Rohde, J. M., Passons, C., Shay, J. W., & Wright, W. E. (2001). Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions. Genes and Development, 15(4), 398-403. https://doi.org/10.1101/gad.859201