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Telomeres, DNA Damage Response and Genomic Instability

The number of dysfunctional telomeres in a cell: one amplifies; more than one translocate

Tusell L. · Soler D. · Agostini M. · Pampalona J. · Genescà A.

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Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Bellaterra (Spain)

Related Articles for ""

Cytogenet Genome Res 122:315–325 (2008)

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Article / Publication Details

First-Page Preview
Abstract of Telomeres, DNA Damage Response and Genomic Instability

Accepted: September 26, 2008
Published online: January 30, 2009
Issue release date: February 2009

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR

Abstract

Chromosomal instability is increasingly appreciated as a key component of tumorigenesis in humans. A combination of abnormal telomere shortening and cell-cycle checkpoint deficiency has been proposed as the initial lesions causing destabilizing chromatin bridges in proliferative cells. We examined the participation of the different types of end-to-end fusions in generating instable karyotypes in non-transformed human breast epithelial cells. We concluded that short dysfunctional telomeres represent an initiating substrate for post-replicative rejoining of sister chromatids and are likely to make an important contribution to the formation of chromosomal rearrangements and the amplification of chromosome arm segments in breast epithelial cells. We propose that there is a chronological order in the participation of the different types of end-to-end fusions in the generation of chromosomal instability. Thus, intrachromosomal post-replicative joining would proceed mainly in the early stages after overcoming growth arrest, when telomere dysfunction is limited and affects only one chromosome end in a cell. The absence of a second substrate for end joining will conduct the cell with the uncapped chromosome to replicate its DNA and fuse the uncapped sister chromatids after replication. Later, since telomeres shorten progressively with each DNA replication round, the uncapping will affect many more chromosome ends, and fusions between the uncapped ends from different chromosomes will be produced. While the fusion of sister chromatids will produce chromosome segment amplification and terminal deletions in the daughter cells, interchromosomal fusion will produce unbalanced rearrangements other than chromosome segment amplifications.

© 2008 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Telomeres, DNA Damage Response and Genomic Instability

Accepted: September 26, 2008
Published online: January 30, 2009
Issue release date: February 2009

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR


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