Short Telomeres, even in the Presence of Telomerase, Limit Tissue Renewal Capacity
Open accessAbstract
Autosomal-dominant dyskeratosis congenita is associated with heterozygous mutations in telomerase. To examine the dosage effect of telomerase, we generated a line of mTR+/- mice on the CAST/EiJ background, which has short telomeres. Interbreeding of heterozygotes resulted in progressive telomere shortening, indicating that limiting telomerase compromises telomere maintenance. In later-generation heterozygotes, we observed a decrease in tissue renewal capacity in the bone marrow, intestines, and testes that resembled defects seen in dyskeratosis congenita patients. The progressive worsening of disease with decreasing telomere length suggests that short telomeres, not telomerase level, cause stem cell failure. Further, wild-type mice derived from the late-generation heterozygous parents, termed wt*, also had short telomeres and displayed a germ cell defect, indicating that telomere length determines these phenotypes. We propose that short telomeres in mice that have normal telomerase levels can cause an occult form of genetic disease.
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The single strand tail length at the 3′ end of telomeres varies between approximately 100 and 280 nucleotides in humans.
“The single strand tail length varies between approximately 100 and 280 nucleotides in humans [12-17].”
From Markers of cellular senescence. Telomere shortening as a marker of cellular senescence (2016) · cites this paper as [14]
Many studies have shown a dependence of telomere length on age: average telomere lengths are shorter in senescent cells than in cells of younger age groups and are also shorter for male than for female.
“Conversely, many studies have shown a dependence of telomere length on age: average telomere lengths are shorter in senescent cells than in cells of younger age groups and are also shorter for male than for female [12-17].”
From Markers of cellular senescence. Telomere shortening as a marker of cellular senescence (2016) · cites this paper as [14]
Mouse studies show that telomere length is inherited as a distinct genotype and can be uncoupled from the telomerase and telomere gene loci.
“When quantified, telomere length is short in wild-type offspring of parent M. castaneus mice that have short telomeres, indicating that telomere length is inherited36,82”
From The telomere syndromes (2012) · cites this paper as [36]
The telomerase-knockout mouse is a valuable model for studying telomere-mediated disease mechanisms because its phenotypes closely match those in humans.
“The telomerase-knockout mouse has provided an important model for understanding telomere-mediated disease mechanisms because there is a remarkable convergence with human disease phenotypes (an overview is shown in Table 2)36,82,84,85,97,99–111.”
From The telomere syndromes (2012) · cites this paper as [36]
Telomere dysfunction causes stem cell failure phenotypes in other tissues, including intestinal epithelium where it manifests as villous atrophy due to loss of crypt stem cells.
“For example, in the intestinal epithelium, it manifests as villous atrophy due to a loss of crypt stem cells36,101,118.”
From The telomere syndromes (2012) · cites this paper as [36]
Even with normal telomerase levels, only a few telomeres are typically elongated in a given cell cycle or generation.
“Even at wild-type levels, telomerase generally elongates only a few telomeres in any given cell cycle or generation34,36.”
From The telomere syndromes (2012) · cites this paper as [36]
In humans and mice, short telomeres cause quantitative and qualitative defects in hematopoietic stem cells, manifesting as stem cell exhaustion.
“In both humans and mice, there is clear evidence that short telomeres cause quantitative and qualitative defects in HSCs, which manifest as stem cell exhaustion36,41,71,114–117 (Fig. 4).”
From The telomere syndromes (2012) · cites this paper as [36]
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- Authors
- Hao, L.-Y., Armanios, M., Strong, M. A., Karim, B., Feldser, D. M., Huso, D., & Greider, C. W.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Greider, Carol W.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2005-12
- Volume
- 123
- Issue
- 6
- Pages
- 1121-1131
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2052066518
- Cited by
- 302
- References
- 49
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- FWCI
- 12.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
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- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
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- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Johns Hopkins University
- National Institutes of Health
- National Cancer Institute (P01CA16519, P01CA016519)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- telomere length, telomerase, dyskeratosis congenita, tissue renewal, telomere shortening, bone marrow, intestine, testis, autosomal dominant inheritance, telomere maintenance
- MeSH terms
- Animals, Blood Cell Count, Crosses, Genetic, Fluorouracil, Genotype, Haplotypes, Hematopoietic System, Heterozygote, Intestinal Mucosa, Intestines, Longevity, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Phenotype, Seminiferous Tubules, Stem Cells, Testis, Time Factors, Survival Rate, Bone Marrow Transplantation, Telomere, Mice, Knockout, Telomerase, Dyskeratosis Congenita, Anticipation, Genetic, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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