A role for the Rb family of proteins in controlling telomere length
Abstract
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. Critically short telomeres and telomeres lacking telomere-binding proteins lose their functionality and are metabolized as DNA breaks, thus generating chromosomal fusions. Telomerase activity is sufficient to rescue short telomeres and confers an unlimited proliferative capacity. In addition, the tumor-suppressor pathway Cdkn2a/Rb1 has also been implicated as a barrier to immortalization. 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.
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The RB family transmits signals that induce senescence in cells with shortened telomeres.
“Furthermore, the RB family controls the length of telomeres and mediates the cellular signals to induce senescence in cells with shortened telomeres125–127.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [125]
The RB family regulates telomere length.
“Furthermore, the RB family controls the length of telomeres and mediates the cellular signals to induce senescence in cells with shortened telomeres125–127.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [125]
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Self-citation
- Authors
- García-Cao, M., Gonzalo, S., Dean, D., & Blasco, M. A.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- Nature Genetics
- Published
- 2002-10-15
- Volume
- 32
- Issue
- 3
- Pages
- 415-419
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W2058285525
- Cited by
- 120
- References
- 30
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 2 · 2022: 6 · 2021: 4 · 2020: 2 · 2019: 8 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 3 · 2012: 12
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- telomere length, retinoblastoma protein, RB1, RBL1, RBL2, telomere elongation, telomerase, telomere capping, chromosome fusion, cellular senescence, cell immortalization, CDKN2A, mouse embryonic fibroblasts, tumor suppression
- MeSH terms
- Animals, Cells, Cultured, Chromosome Aberrations, Chromosomes, DNA, Fibroblasts, Flow Cytometry, Genotype, Mice, Inbred C57BL, Microscopy, Fluorescence, Nuclear Proteins, Retinoblastoma Protein, Telomere, In Situ Hybridization, Fluorescence, Mice, Knockout, Telomerase, Retinoblastoma-Like Protein p107, Mice
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