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A role for the Rb family of proteins in controlling telomere length
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Journal Article
A role for the Rb family of proteins in controlling telomere length
2002
Overview
The molecular mechanisms of cellular mortality have recently begun to be unraveled. In particular, it has been discovered that cells that lack telomerase are subject to telomere attrition with each round of replication, eventually leading to loss of telomere capping function at chromosome ends
1
,
2
,
3
,
4
,
5
. Critically short telomeres and telomeres lacking telomere-binding proteins lose their functionality and are metabolized as DNA breaks, thus generating chromosomal fusions
1
,
2
,
3
,
4
,
5
,
6
,
7
,
8
. Telomerase activity is sufficient to rescue short telomeres and confers an unlimited proliferative capacity
9
,
10
,
11
. In addition, the tumor-suppressor pathway Cdkn2a/Rb1 has also been implicated as a barrier to immortalization
12
,
13
,
14
. Here, we report a connection between the members of the retinoblastoma family of proteins, Rb1 (retinoblastoma 1), Rbl1 (retinoblastoma-like 1) and Rbl2 (retinoblastoma-like 2), and the mechanisms that regulate telomere length. In particular, mouse embryonic fibroblasts doubly deficient in
Rbl1
and
Rbl2
or triply deficient in
Rbl1
,
Rbl2
and
Rb1
have markedly elongated telomeres compared with those of wildtype or
Rb1
-deficient cells. This deregulation of telomere length is not associated with increased telomerase activity. Notably, the abnormally elongated telomeres in doubly or triply deficient cells retain their end-capping function, as shown by the normal frequency of chromosomal fusions. These findings demonstrate a connection between the Rb1 family and the control of telomere length in mammalian cells.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animal Genetics and Genomics
/ Animals
/ Biological and medical sciences
/ Biomedical and Life Sciences
/ Chromosomes - ultrastructure
/ DNA
/ Fundamental and applied biological sciences. Psychology
/ Genotype
/ In Situ Hybridization, Fluorescence
/ letter
/ Mammals
/ Mice
/ Molecular and cellular biology
/ Nuclear Proteins - metabolism
/ Nuclear Proteins - physiology
/ Oncology
/ Proteins
/ Retinoblastoma Protein - metabolism
/ Retinoblastoma Protein - physiology
/ Retinoblastoma-Like Protein p107
/ Yeast
