ArticleDisease models & mechanisms
Telomerase reverse transcriptase-dependent telomere equilibration mitigates tissue dysfunction in mTert heterozygotes.
Article in Disease models & mechanisms. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Modification of the telomerase gene with human regulatory sequences resets mouse telomeres to human length.Nature communications · 2025Article
- Humanization of the mouseResearch square · 2024Article
- Tieing together loose ends: telomere instability in cancer and aging.Molecular oncology · 2022Review
- Transient induction of telomerase expression mediates senescence and reduces tumorigenesis in primary fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Telomerase Mediates Lymphocyte Proliferation but Not the Atherosclerosis-Suppressive Potential of Regulatory T-Cells.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Review
- A method for measuring the distribution of the shortest telomeres in cells and tissues.Nature communications · 2017Article
- Short Telomeres in Key Tissues Initiate Local and Systemic Aging in Zebrafish.PLoS genetics · 2016Article
- Telomerase is required for zebrafish lifespan.PLoS genetics · 2013Article
- Long telomeres bypass the requirement for telomere maintenance in human tumorigenesis.Cell reports · 2012Article
- Phenotypes in mTERT⁺/⁻ and mTERT⁻/⁻ mice are due to short telomeres, not telomere-independent functions of telomerase reverse transcriptase.Molecular and cellular biology · 2011Article
- Telomere length is inherited with resetting of the telomere set-point.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
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Abstract
Autosomal dominant mutations in telomere-associated factors elicit a disease known as dyskeratosis congenita (DKC), and patients suffer proliferative abnormalities associated with telomere erosion. Mice that are heterozygous for telomerase genes (Tert or Terc, hereafter referred to as mTert and mTerc) are useful models of telomerase haploinsufficiency, but do not strictly mimic DKC. In strains with long telomeres (>60 kbp), animals that are heterozygous for mTert undergo telomere erosion for nine generations and remain phenotypically normal. In an mTerc heterozygous strain with short telomeres (<15 kbp), early mortality arises after five to six generations, but dyskeratosis occurs only upon the further loss of mPot1b. We show that prolonged mTert heterozygosity (for greater than ten generations) did not elicit disease, even upon heterozygote interbreeding, and that telomeres reset to wild-type lengths. This lengthening did not occur in nullizygotes, and short telomeres inherited from mTert null parents were rescued only in heterozygous progeny. In the bone marrow, nullizygotes remained competent for radioprotection for three generations. Thus, gradual telomere erosion in the presence of telomerase may enable subsequent telomere extension, similar to that described in budding yeast. We speculate whether such adaptation occurs in normal human cells (or whether it could be induced in DKC-derived cells), and whether it might mitigate the impact of telomerase inhibition upon stem cells during cancer therapy.
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