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Human Molecular Genetics, 2003, Vol. 12, No. 11 1329-1336
DOI: 10.1093/hmg/ddg139
© 2003 Oxford University Press

Telomere length and the expression of natural telomeric genes in human fibroblasts

Yi Ning1,*, Jing-fan Xu1, Yu Li2, Liz Chavez3, Harold C. Riethman4, Peter M. Lansdorp3 and Nan-ping Weng2

1Department of Pathology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA, 2Laboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA, 3Terry-Fox Laboratory, BC Cancer Research Centre, Vancouver, British Columbia, Canada V5Z 1L3 and 4The Wistar Institute, Philadelphia, PA 19104, USA

Received December 20, 2002; Revised February 20, 2003; Accepted March 30, 2003

Progressive telomere shortening occurs with division of normal human cells, and eventually leads to replicative senescence. The mechanism by which the shortened telomeres cause growth arrest is largely unknown. Transcriptional silencing of genes adjacent to telomeres, also called telomere position effect, has been hypothesized as a possible mechanism of telomere-mediated senescence. However, there is no report regarding telomere position effect on natural telomeric genes in human cells. To address whether the expression of natural telomeric genes is regulated by telomere length, we combined quantitative RT–PCR with quantitative fluorescence in situ hybridization to comparatively analyze the expression of 34 telomeric genes and telomere length of their 24 corresponding chromosome ends in young and senescent human fibroblasts. We have demonstrated here that telomere length alone is not sufficient to determine the expression status of natural telomeric genes. An extended analysis of a tandem of eight telomeric genes on a single chromosome end revealed a discontinuous pattern of changed expression during telomere shortening and some of the changes are senescence-specific rather than non-dividing-related. These results suggest that the expression of natural telomeric genes may be influenced by alteration of local heterochromatin structure.

* To whom correspondence should be addressed. Tel: +1 4107061282; Fax: +1 4107068414; Email: yning{at}som.umaryland.edu


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