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Artykuły w czasopismach na temat „Telomeres”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Brault, Marie Eve, and Chantal Autexier. "Telomeric recombination induced by dysfunctional telomeres." Molecular Biology of the Cell 22, no. 2 (2011): 179–88. http://dx.doi.org/10.1091/mbc.e10-02-0173.

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Telomere maintenance is essential for cellular immortality, and most cancer cells maintain their telomeres through the enzyme telomerase. Telomeres and telomerase represent promising anticancer targets. However, 15% of cancer cells maintain their telomeres through alternative recombination-based mechanisms, and previous analyses showed that recombination-based telomere maintenance can be activated after telomerase inhibition. We determined whether telomeric recombination can also be promoted by telomere dysfunction. We report for the first time that telomeric recombination can be induced in hu

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Lin, Chi-Ying, Hsih-Hsuan Chang, Kou-Juey Wu та ін. "Extrachromosomal Telomeric Circles Contribute to Rad52-, Rad50-, and Polymerase δ-Mediated Telomere-Telomere Recombination in Saccharomyces cerevisiae". Eukaryotic Cell 4, № 2 (2005): 327–36. http://dx.doi.org/10.1128/ec.4.2.327-336.2005.

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ABSTRACT Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the telomerase reverse transcriptase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. By using an in vivo inducible Cre-loxP system to generate and trace the fate of marked telomeric DNA-containing rings, the efficiency of telomere-telomere recombination can be determined quantitatively. We show that the telomeric loci are the primary sites at which a marked telomeric ring-containing DNA is observed among wild-type

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3

Bechard, Laura H., Bilge D. Butuner, George J. Peterson, Will McRae, Zeki Topcu, and Michael J. McEachern. "Mutant Telomeric Repeats in Yeast Can Disrupt the Negative Regulation of Recombination-Mediated Telomere Maintenance and Create an Alternative Lengthening of Telomeres-Like Phenotype." Molecular and Cellular Biology 29, no. 3 (2008): 626–39. http://dx.doi.org/10.1128/mcb.00423-08.

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ABSTRACT Some human cancers maintain telomeres using alternative lengthening of telomeres (ALT), a process thought to be due to recombination. In Kluyveromyces lactis mutants lacking telomerase, recombinational telomere elongation (RTE) is induced at short telomeres but is suppressed once telomeres are moderately elongated by RTE. Recent work has shown that certain telomere capping defects can trigger a different type of RTE that results in much more extensive telomere elongation that is reminiscent of human ALT cells. In this study, we generated telomeres composed of either of two types of mu

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4

Kondratieva, Yu A., and L. P. Mendeleeva. "Characteristics of telomere length in patients with hematological diseases (literature review)." Oncohematology 16, no. 1 (2021): 23–30. http://dx.doi.org/10.17650/1818-8346-2021-16-1-23-30.

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Telomeres are protein structures that regulate the process of cellular aging and play the role of a protective “cap” on the end sections of chromosomes. The telomeres of nucleated cells undergo permanent shortening during their lifetime as a result of multiple cycles of DNA replication. The enzyme that provides completion of the missing telomeric repeats at the ends of chromosomes is called “telomerase”. However, recovery of critically short telomeres by telomerase or recombination in somatic cells is limited due to the presence of a large accumulation of unclosed telomeres, which triggers apo

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5

Basenko, Evelina, Zeki Topcu, and Michael J. McEachern. "Recombination Can either Help Maintain Very Short Telomeres or Generate Longer Telomeres in Yeast Cells with Weak Telomerase Activity." Eukaryotic Cell 10, no. 8 (2011): 1131–42. http://dx.doi.org/10.1128/ec.05079-11.

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ABSTRACT Yeast mutants lacking telomerase are able to elongate their telomeres through processes involving homologous recombination. In this study, we investigated telomeric recombination in several mutants that normally maintain very short telomeres due to the presence of a partially functional telomerase. The abnormal colony morphology present in some mutants was correlated with especially short average telomere length and with a requirement for RAD52 for indefinite growth. Better-growing derivatives of some of the mutants were occasionally observed and were found to have substantially elong

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6

Cook, Brandoch D., Jasmin N. Dynek, William Chang, Grigoriy Shostak, and Susan Smith. "Role for the Related Poly(ADP-Ribose) Polymerases Tankyrase 1 and 2 at Human Telomeres." Molecular and Cellular Biology 22, no. 1 (2002): 332–42. http://dx.doi.org/10.1128/mcb.22.1.332-342.2002.

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ABSTRACT Telomere maintenance is essential for the continuous growth of tumor cells. In most human tumors telomeres are maintained by telomerase, a specialized reverse transcriptase. Tankyrase 1, a human telomeric poly(ADP-ribose) polymerase (PARP), positively regulates telomere length through its interaction with TRF1, a telomeric DNA-binding protein. Tankyrase 1 ADP-ribosylates TRF1, inhibiting its binding to telomeric DNA. Overexpression of tankyrase 1 in the nucleus promotes telomere elongation, suggesting that tankyrase 1 regulates access of telomerase to the telomeric complex. The recent

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7

Perera, Omesha N., Alexander P. Sobinoff, Erdahl T. Teber, et al. "Telomerase promotes formation of a telomere protective complex in cancer cells." Science Advances 5, no. 10 (2019): eaav4409. http://dx.doi.org/10.1126/sciadv.aav4409.

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Telomerase is a ribonucleoprotein complex that catalyzes addition of telomeric DNA repeats to maintain telomeres in replicating cells. Here, we demonstrate that the telomerase protein hTERT performs an additional role at telomeres that is independent of telomerase catalytic activity yet essential for telomere integrity and cell proliferation. Short-term depletion of endogenous hTERT reduced the levels of heat shock protein 70 (Hsp70-1) and the telomere protective protein Apollo at telomeres, and induced telomere deprotection and cell cycle arrest, in the absence of telomere shortening. Short-t

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8

Chan, Simon R. W. L., and Elizabeth H. Blackburn. "Telomeres and telomerase." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (2004): 109–22. http://dx.doi.org/10.1098/rstb.2003.1370.

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Telomeres are the protective DNA–protein complexes found at the ends of eukaryotic chromosomes. Telomeric DNA consists of tandem repeats of a simple, often G–rich, sequence specified by the action of telomerase, and complete replication of telomeric DNA requires telomerase. Telomerase is a specialized cellular ribonucleoprotein reverse transcriptase. By copying a short template sequence within its intrinsic RNA moiety, telomerase synthesizes the telomeric DNA strand running 5' to 3' towards the distal end of the chromosome, thus extending it. Fusion of a telomere, either with another telomere

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9

Dreesen, Oliver, and George A. M. Cross. "Telomerase-Independent Stabilization of Short Telomeres in Trypanosoma brucei." Molecular and Cellular Biology 26, no. 13 (2006): 4911–19. http://dx.doi.org/10.1128/mcb.00212-06.

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ABSTRACT In cancer cells and germ cells, shortening of chromosome ends is prevented by telomerase. Telomerase-deficient cells have a replicative life span, after which they enter senescence. Senescent cells can give rise to survivors that maintain chromosome ends through recombination-based amplification of telomeric or subtelomeric repeats. We found that in Trypanosoma brucei, critically short telomeres are stable in the absence of telomerase. Telomere stabilization ensured genomic integrity and could have implications for telomere maintenance in human telomerase-deficient cells. Cloning and

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10

Kishtagari, Ashwin, and Justin Watts. "Biological and clinical implications of telomere dysfunction in myeloid malignancies." Therapeutic Advances in Hematology 8, no. 11 (2017): 317–26. http://dx.doi.org/10.1177/2040620717731549.

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Telomeres at the ends of linear chromosomes protect the genome. Telomeres shorten with each round of cell division, placing a finite limit on cell growth. Telomere attrition is associated with cell senescence and apoptosis. Telomerase, a specialized ribonucleoprotein complex, maintains telomeres homeostasis through repeat addition of telomere sequences to the 3′ telomeric overhang. Telomere biology is closely related to cancer and normal aging. Upregulation of telomerase or activation of the alternative pathway of telomere lengthening is a hallmark of cancer cells, making telomerase an attract

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11

Mondello, Chiara, and A. Ivana Scovassi. "Telomeres, telomerase, and apoptosis." Biochemistry and Cell Biology 82, no. 4 (2004): 498–507. http://dx.doi.org/10.1139/o04-048.

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Telomeres are specialized high-order chromatin structures that cap the ends of eukaryotic chromosomes. In vertebrates, telomeric DNA is composed of repetitions of the TTAGGG hexanucleotide, is bound to a set of specific proteins, and is elongated by the reverse transcriptase enzyme telomerase. Telomerase activity is promptly detected in cells with an indefinite replicative potential, such as cancer cells, while is almost undetectable in normal cells, which are characterized by a limited life span. Mounting evidence indicates that the maintenance of telomere integrity and telomerase protect cel

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12

Marchesini, M., R. Matocci, L. Tasselli, et al. "PML is required for telomere stability in non-neoplastic human cells." Oncogene 35, no. 14 (2015): 1811–21. http://dx.doi.org/10.1038/onc.2015.246.

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Abstract Telomeres interact with numerous proteins, including components of the shelterin complex, whose alteration, similarly to proliferation-induced telomere shortening, initiates cellular senescence. In tumors, telomere length is maintained by Telomerase activity or by the Alternative Lengthening of Telomeres mechanism, whose hallmark is the telomeric localization of the promyelocytic leukemia (PML) protein. Whether PML contributes to telomeres maintenance in normal cells is unknown. We show that in normal human fibroblasts the PML protein associates with few telomeres, preferentially when

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13

Cohn, Marita, Ahu Karademir Andersson, Raquel Quintilla Mateo, and Mirja Carlsson Möller. "Alternative Lengthening of Telomeres in the Budding Yeast Naumovozyma castellii." G3: Genes|Genomes|Genetics 9, no. 10 (2019): 3345–58. http://dx.doi.org/10.1534/g3.119.400428.

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The enzyme telomerase ensures the integrity of linear chromosomes by maintaining telomere length. As a hallmark of cancer, cell immortalization and unlimited proliferation is gained by reactivation of telomerase. However, a significant fraction of cancer cells instead uses alternative telomere lengthening mechanisms to ensure telomere function, collectively known as Alternative Lengthening of Telomeres (ALT). Although the budding yeast Naumovozyma castellii (Saccharomyces castellii) has a proficient telomerase activity, we demonstrate here that telomeres in N. castellii are efficiently maintai

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14

Jády, Beáta E., Patricia Richard, Edouard Bertrand, and Tamás Kiss. "Cell Cycle-dependent Recruitment of Telomerase RNA and Cajal Bodies to Human Telomeres." Molecular Biology of the Cell 17, no. 2 (2006): 944–54. http://dx.doi.org/10.1091/mbc.e05-09-0904.

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Telomerase is a ribonucleoprotein enzyme that counteracts replicative telomere erosion by adding telomeric sequence repeats onto chromosome ends. Despite its well-established role in telomere synthesis, telomerase has not yet been detected at telomeres. The RNA component of human telomerase (hTR) resides in the nucleoplasmic Cajal bodies (CBs) of interphase cancer cells. Here, in situ hybridization demonstrates that in human HeLa and Hep2 S phase cells, besides accumulating in CBs, hTR specifically concentrates at a few telomeres that also accumulate the TRF1 and TRF2 telomere marker proteins.

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15

Fernandes, Stina George, Rebecca Dsouza, Gouri Pandya, et al. "Role of Telomeres and Telomeric Proteins in Human Malignancies and Their Therapeutic Potential." Cancers 12, no. 7 (2020): 1901. http://dx.doi.org/10.3390/cancers12071901.

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Telomeres are the ends of linear chromosomes comprised of repetitive nucleotide sequences in humans. Telomeres preserve chromosomal stability and genomic integrity. Telomere length shortens with every cell division in somatic cells, eventually resulting in replicative senescence once telomere length becomes critically short. Telomere shortening can be overcome by telomerase enzyme activity that is undetectable in somatic cells, while being active in germline cells, stem cells, and immune cells. Telomeres are bound by a shelterin complex that regulates telomere lengthening as well as protects t

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16

Ji, Hong, Christopher J. Adkins, Bethany R. Cartwright, and Katherine L. Friedman. "Yeast Est2p Affects Telomere Length by Influencing Association of Rap1p with Telomeric Chromatin." Molecular and Cellular Biology 28, no. 7 (2008): 2380–90. http://dx.doi.org/10.1128/mcb.01648-07.

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ABSTRACT In Saccharomyces cerevisiae, the sequence-specific binding of the negative regulator Rap1p provides a mechanism to measure telomere length: as the telomere length increases, the binding of additional Rap1p inhibits telomerase activity in cis. We provide evidence that the association of Rap1p with telomeric DNA in vivo occurs in part by sequence-independent mechanisms. Specific mutations in EST2 (est2-LT) reduce the association of Rap1p with telomeric DNA in vivo. As a result, telomeres are abnormally long yet bind an amount of Rap1p equivalent to that observed at wild-type telomeres.

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17

Natarajan, Shobhana, Cindy Groff-Vindman, and Michael J. McEachern. "Factors Influencing the Recombinational Expansion and Spread of Telomeric Tandem Arrays in Kluyveromyces lactis." Eukaryotic Cell 2, no. 5 (2003): 1115–27. http://dx.doi.org/10.1128/ec.2.5.1115-1127.2003.

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ABSTRACT We have previously shown that DNA circles containing telomeric repeats and a marker gene can promote the recombinational elongation of telomeres in Kluyveromyces lactis by a mechanism proposed to involve rolling-circle DNA synthesis. Wild-type cells acquire a long tandem array at a single telomere, while telomerase deletion (ter1-Δ) cells, acquire an array and also spread it to multiple telomeres. In this study, we further examine the factors that affect the formation and spread of telomeric tandem arrays. We show that a telomerase+ strain with short telomeres and high levels of subte

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18

Choe, Wonchae, Martin Budd, Osamu Imamura, Laura Hoopes, and Judith L. Campbell. "Dynamic Localization of an Okazaki Fragment Processing Protein Suggests a Novel Role in Telomere Replication." Molecular and Cellular Biology 22, no. 12 (2002): 4202–17. http://dx.doi.org/10.1128/mcb.22.12.4202-4217.2002.

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ABSTRACT We have found that the Dna2 helicase-nuclease, thought to be involved in maturation of Okazaki fragments, is a component of telomeric chromatin. We demonstrate a dynamic localization of Dna2p to telomeres that suggests a dual role for Dna2p, one in telomere replication and another, unknown function, perhaps in telomere capping. Both chromatin immunoprecipitation (ChIP) and immunofluorescence show that Dna2p associates with telomeres but not bulk chromosomal DNA in G1 phase, when there is no telomere replication and the telomere is transcriptionally silenced. In S phase, there is a dra

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19

Eberhard, Stephan, Sona Valuchova, Julie Ravat, et al. "Molecular characterization of Chlamydomonas reinhardtii telomeres and telomerase mutants." Life Science Alliance 2, no. 3 (2019): e201900315. http://dx.doi.org/10.26508/lsa.201900315.

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Telomeres are repeated sequences found at the end of the linear chromosomes of most eukaryotes and are required for chromosome integrity. Expression of the reverse-transcriptase telomerase allows for extension of telomeric repeats to counteract natural telomere shortening. Although Chlamydomonas reinhardtii, a photosynthetic unicellular green alga, is widely used as a model organism in photosynthesis and flagella research, and for biotechnological applications, the biology of its telomeres has not been investigated in depth. Here, we show that the C. reinhardtii (TTTTAGGG)n telomeric repeats a

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20

Underwood, Dana H., Coleen Carroll, and Michael J. McEachern. "Genetic Dissection of the Kluyveromyces lactis Telomere and Evidence for Telomere Capping Defects in TER1 Mutants with Long Telomeres." Eukaryotic Cell 3, no. 2 (2004): 369–84. http://dx.doi.org/10.1128/ec.3.2.369-384.2004.

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ABSTRACT In the yeast Kluyveromyces lactis, the telomeres are composed of perfect 25-bp repeats copied from a 30-nucleotide RNA template defined by 5-nucleotide terminal repeats. A genetic dissection of the K. lactis telomere was performed by using mutant telomerase RNA (TER1) alleles to incorporate mutated telomeric repeats. This analysis has shown that each telomeric repeat contains several functional regions, some of which may physically overlap. Mutations in the terminal repeats of the template RNA typically lead to telomere shortening, as do mutations in the right side of the Rap1p bindin

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Kelleher, Colleen, Isabel Kurth, and Joachim Lingner. "Human Protection of Telomeres 1 (POT1) Is a Negative Regulator of Telomerase Activity In Vitro." Molecular and Cellular Biology 25, no. 2 (2005): 808–18. http://dx.doi.org/10.1128/mcb.25.2.808-818.2005.

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ABSTRACT The telomeric single-strand DNA binding protein protection of telomeres 1 (POT1) protects telomeres from rapid degradation in Schizosaccharomyces pombe and has been implicated in positive and negative telomere length regulation in humans. Human POT1 appears to interact with telomeres both through direct binding to the 3′ overhanging G-strand DNA and through interaction with the TRF1 duplex telomere DNA binding complex. The influence of POT1 on telomerase activity has not been studied at the molecular level. We show here that POT1 negatively effects telomerase activity in vitro. We fin

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22

Prescott, John C., and Elizabeth H. Blackburn. "Telomerase RNA Template Mutations Reveal Sequence-Specific Requirements for the Activation and Repression of Telomerase Action at Telomeres." Molecular and Cellular Biology 20, no. 8 (2000): 2941–48. http://dx.doi.org/10.1128/mcb.20.8.2941-2948.2000.

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ABSTRACT Telomeric DNA is maintained within a length range characteristic of an organism or cell type. Significant deviations outside this range are associated with altered telomere function. The yeast telomere-binding protein Rap1p negatively regulates telomere length. Telomere elongation is responsive to both the number of Rap1p molecules bound to a telomere and the Rap1p-centered DNA-protein complex at the extreme telomeric end. Previously, we showed that a specific trinucleotide substitution in the Saccharomyces cerevisiae telomerase gene (TLC1) RNA template abolished the enzymatic activit

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23

Schaetzlein, S., and K. L. Rudolph. "Telomere length regulation during cloning, embryogenesis and ageing." Reproduction, Fertility and Development 17, no. 2 (2005): 85. http://dx.doi.org/10.1071/rd04112.

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Telomeres are nucleoprotein complexes at the end of eukaryotic chromosomes with an essential role in chromosome capping. Owing to the end-replication problem of DNA polymerase, telomeres shorten during each cell division. When telomeres become critically short, they loose their capping function, which in turn induces a DNA damage-like response. This mechanism inhibits cell proliferation at the senescence stage and there is evidence that it limits the regenerative capacity of tissues and organs during chronic diseases and ageing. The holoenzyme telomerase synthesises telomeric DNA de novo, but,

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24

Henderson, S., R. Allsopp, D. Spector, S. S. Wang, and C. Harley. "In situ analysis of changes in telomere size during replicative aging and cell transformation." Journal of Cell Biology 134, no. 1 (1996): 1–12. http://dx.doi.org/10.1083/jcb.134.1.1.

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Telomeres have been shown to gradually shorten during replicative aging in human somatic cells by Southern analysis. This study examines telomere shortening at the single cell level by fluorescence in situ hybridization (FISH). FISH and confocal microscopy of interphase human diploid fibroblasts (HDFs) demonstrate that telomeres are distributed throughout the nucleus with an interchromosomal heterogeneity in size. Analysis of HDFs at increasing population doubling levels shows a gradual increase in spot size, intensity, and detectability of telomeric signal. FISH of metaphase chromosomes prepa

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Smogorzewska, Agata, Bas van Steensel, Alessandro Bianchi, et al. "Control of Human Telomere Length by TRF1 and TRF2." Molecular and Cellular Biology 20, no. 5 (2000): 1659–68. http://dx.doi.org/10.1128/mcb.20.5.1659-1668.2000.

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ABSTRACT Telomere length in human cells is controlled by a homeostasis mechanism that involves telomerase and the negative regulator of telomere length, TRF1 (TTAGGG repeat binding factor 1). Here we report that TRF2, a TRF1-related protein previously implicated in protection of chromosome ends, is a second negative regulator of telomere length. Overexpression of TRF2 results in the progressive shortening of telomere length, similar to the phenotype observed with TRF1. However, while induction of TRF1 could be maintained over more than 300 population doublings and resulted in stable, short tel

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Donate, Luis E., and Maria A. Blasco. "Telomeres in cancer and ageing." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1561 (2011): 76–84. http://dx.doi.org/10.1098/rstb.2010.0291.

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Telomeres protect the chromosome ends from unscheduled DNA repair and degradation. Telomeres are heterochromatic domains composed of repetitive DNA (TTAGGG repeats) bound to an array of specialized proteins. The length of telomere repeats and the integrity of telomere-binding proteins are both important for telomere protection. Furthermore, telomere length and integrity are regulated by a number of epigenetic modifications, thus pointing to higher order control of telomere function. In this regard, we have recently discovered that telomeres are transcribed generating long, non-coding RNAs, whi

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Schmidt, Tobias T., Carly Tyer, Preeyesh Rughani, et al. "Abstract 1639: Telomere dynamics in aging and cancer by nanopore long-read sequencing." Cancer Research 84, no. 6_Supplement (2024): 1639. http://dx.doi.org/10.1158/1538-7445.am2024-1639.

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Abstract Telomeres are the protective, nucleoprotein structure at the ends of linear eukaryotic chromosomes. The accurate measurement of both telomeric length and composition of individual telomeres in mammalian cells has been challenged by the length and repetitive nature of telomeres. With the advent of third generation sequencing technologies, it is now technically possible to sequence entire telomeres and map them to individual chromosome arms. Here, we report a reliable method to enrich, sequence and analyze human telomeres using Oxford Nanopore Technologies long-read sequencing. To enric

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Stock, Carmel J. W., and Elisabetta A. Renzoni. "Telomeres in Interstitial Lung Disease." Journal of Clinical Medicine 10, no. 7 (2021): 1384. http://dx.doi.org/10.3390/jcm10071384.

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Interstitial lung diseases (ILD) encompass a group of conditions involving fibrosis and/or inflammation of the pulmonary parenchyma. Telomeres are repetitive DNA sequences at chromosome ends which protect against genome instability. At each cell division, telomeres shorten, but the telomerase complex partially counteracts progressive loss of telomeres by catalysing the synthesis of telomeric repeats. Once critical telomere shortening is reached, cell cycle arrest or apoptosis are triggered. Telomeres progressively shorten with age. A number of rare genetic mutations have been identified in gen

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Hahn, William C. "Role of Telomeres and Telomerase in the Pathogenesis of Human Cancer." Journal of Clinical Oncology 21, no. 10 (2003): 2034–43. http://dx.doi.org/10.1200/jco.2003.06.018.

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Specialized nucleoprotein structures, termed telomeres, cap the ends of human chromosomes. These terminal structures, composed of repetitive arrays of guanine-rich hexameric DNA together with specific telomere-binding proteins, play essential roles in protecting the chromosome from damage and degradation. In addition, several lines of evidence implicate telomere maintenance as an important regulator of cell life span. Activation of telomerase, a dedicated reverse transcriptase that synthesizes telomeric sequences, is strongly associated with cancer, and recent observations confirm that telomer

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Natarajan, Shobhana, and Michael J. McEachern. "Recombinational Telomere Elongation Promoted by DNA Circles." Molecular and Cellular Biology 22, no. 13 (2002): 4512–21. http://dx.doi.org/10.1128/mcb.22.13.4512-4521.2002.

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ABSTRACT Yeast mutants lacking telomerase are capable of maintaining telomeres by an alternate mechanism that depends on homologous recombination. We show here, by using Kluyveromyces lactis cells containing two types of telomeric repeats, that recombinational telomere elongation generates a repeating pattern common in most or all telomeres in survivors that retain both repeat types. We propose that these patterns arise from small circles of telomeric DNA being used as templates for rolling-circle gene conversion and that the sequence from the lengthened telomere is spread to other telomeres b

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Bessler, Monica, Rachida Bouharich, Shashikant Kulkarni, et al. "Accelerated Shortening of Long Telomeres and Accumulation of Short Telomeres in Dyskeratosis Congenita." Blood 106, no. 11 (2005): 1053. http://dx.doi.org/10.1182/blood.v106.11.1053.1053.

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Abstract Dyskeratosis congenita (DC) is the first human disease whose pathogenesis has been directly linked to an impairment of telomere maintenance. Telomeres protect chromosome ends from end to end fusion and degradation. Loss of telomere function causes cell cycle arrest or cell death. Telomeres are maintained by the telomerase ribonucloprotein complex whose integral RNA component, the telomerase RNA or TERC RNA, contains the sequences that act as a template for the synthesis of telomeric repeats. Autosomal dominant DC (AD DC), a rare inherited bone marrow failure syndrome, is caused by mut

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Li, Bibo, and Titia de Lange. "Rap1 Affects the Length and Heterogeneity of Human Telomeres." Molecular Biology of the Cell 14, no. 12 (2003): 5060–68. http://dx.doi.org/10.1091/mbc.e03-06-0403.

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Telomere length is controlled in part by cis-acting negative regulators that limit telomere extension by telomerase. In budding yeast, the major telomere length regulator scRap1 binds to telomeric DNA and acts to inhibit telomere elongation in cis. Because the human Rap1 ortholog hRap1 does not bind to telomeric DNA directly but is recruited to telomeres by TRF2, we examined its role in telomere length control. The data are consistent with hRap1 being a negative regulator of telomere length, indicating functional conservation. Deletion mapping confirmed that hRap1 is tethered to telomeres thro

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McEachern, M. J., and J. B. Hicks. "Unusually large telomeric repeats in the yeast Candida albicans." Molecular and Cellular Biology 13, no. 1 (1993): 551–60. http://dx.doi.org/10.1128/mcb.13.1.551-560.1993.

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We have identified sequences at the telomeres of the yeast Candida albicans and have found that they are composed of tandem copies of a 23-bp sequence. Through the cloning of native telomeric ends and the characterization and cloning of a "healed" end, we demonstrate that these repeated sequences are sufficient to function as a telomere. All copies of the 23-bp repeat that have been sequenced from a number of C. albicans strains are identical. In contrast, adjacent subtelomeric sequences are variable both between strains and within the WO-1 strain. In the WO-1 strain, the lengths of the telome

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McEachern, M. J., and J. B. Hicks. "Unusually large telomeric repeats in the yeast Candida albicans." Molecular and Cellular Biology 13, no. 1 (1993): 551–60. http://dx.doi.org/10.1128/mcb.13.1.551.

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We have identified sequences at the telomeres of the yeast Candida albicans and have found that they are composed of tandem copies of a 23-bp sequence. Through the cloning of native telomeric ends and the characterization and cloning of a "healed" end, we demonstrate that these repeated sequences are sufficient to function as a telomere. All copies of the 23-bp repeat that have been sequenced from a number of C. albicans strains are identical. In contrast, adjacent subtelomeric sequences are variable both between strains and within the WO-1 strain. In the WO-1 strain, the lengths of the telome

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Feigon, Juli. "Structural biology of telomerase mechanism and interactions at telomeres." Structural Dynamics 12, no. 2_Supplement (2025): A201. https://doi.org/10.1063/4.0000509.

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Telomerase is a unique RNA-containing reverse transcriptase that synthesizes the DNA at the 3’-ends of telomeres, the structures at the ends of linear chromosomes. It is a highly regulated determinant of tumorigenesis, cellular aging, and stem cell renewal. All telomerases contain a catalytic core comprising telomerase reverse transcriptase (TERT) and telomerase RNA (TER), along with other proteins involved in biogenesis, assembly, and activation. TER includes a template complementary to ∼1.5 telomere repeats used by TERT to repetitively synthesize the telomere repeat (dTTGGGG in Tetrahymena,

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Datta, Neelabh. "Unravelling the Intricacies of Telomere Replication: A Molecular Conundrum." Canadian Journal for the Academic Mind 2, no. 1 (2024): 97–127. http://dx.doi.org/10.25071/2817-5344/74.

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Telomeres are specialized structures at the ends of linear chromosomes that protect them from degradation and fusion. It’s replication is a complex process that involves both DNA polymerases and a specialized enzyme called telomerase which is a ribonucleoprotein complex that synthesizes telomeric DNA by using an internal RNA template. However, telomerase alone cannot fully replicate the telomeric DNA, and requires the cooperation of other factors, such as shelterin, CST, and DNA repair proteins. Telomere replication is tightly regulated by various mechanisms, such as cell cycle checkpoints, te

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Smith, Christopher D., and Elizabeth H. Blackburn. "Uncapping and Deregulation of Telomeres Lead to Detrimental Cellular Consequences in Yeast." Journal of Cell Biology 145, no. 2 (1999): 203–14. http://dx.doi.org/10.1083/jcb.145.2.203.

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Telomeres are the protein–nucleic acid structures at the ends of eukaryote chromosomes. Tandem repeats of telomeric DNA are templated by the RNA component (TER1) of the ribonucleoprotein telomerase. These repeats are bound by telomere binding proteins, which are thought to interact with other factors to create a higher-order cap complex that stabilizes the chromosome end. In the budding yeast Kluyveromyces lactis, the incorporation of certain mutant DNA sequences into telomeres leads to uncapping of telomeres, manifested by dramatic telomere elongation and increased length heterogeneity (telom

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Han, Xuesheng, Alice Hirschel, Menelaos Tsapekos, Diego Perez, and David Vollmer. "In Vitro Assessment of Gold Nanoparticles on Telomerase Activity and Telomere Length in Human Fibroblasts." International Journal of Molecular Sciences 24, no. 18 (2023): 14273. http://dx.doi.org/10.3390/ijms241814273.

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Telomerase activity coincides with lengthening of the ends of chromosomes known as telomeres. Telomere length is used as a marker for cellular aging. Telomeres shorten over time as cells divide, and certain bioactive compounds such as gold nanoparticles (AuNPs) may slow the shortening of telomeres by increasing telomerase activity. The objective of the present study is to assess the effect of AuNPs on telomerase activity and telomere length in human fibroblasts. Telomerase activity was measured using enzyme-linked immunosorbent assay (ELISA) in primary human lung fibroblasts (IMR90) and using

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Smolikov, Sarit, and Anat Krauskopf. "The Rap1p-Telomere Complex Does Not Determine the Replicative Capacity of Telomerase-Deficient Yeast." Molecular and Cellular Biology 23, no. 23 (2003): 8729–39. http://dx.doi.org/10.1128/mcb.23.23.8729-8739.2003.

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ABSTRACT Telomeres are nucleoprotein structures that cap the ends of chromosomes and thereby protect their stability and integrity. In the presence of telomerase, the enzyme that synthesizes telomeric repeats, telomere length is controlled primarily by Rap1p, the budding yeast telomeric DNA binding protein which, through its C-terminal domain, nucleates a protein complex that limits telomere lengthening. In the absence of telomerase, telomeres shorten with every cell division, and eventually, cells enter replicative senescence. We have set out to identify the telomeric property that determines

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Calado, Rodrigo T., Solomon A. Graf, and Neal S. Young. "Telomeric Recombination in Lymphocytes Implicates ALT, an Alternative Mechanism for Telomere Length Maintenance, in Normal Human Hematopoietic Cells." Blood 110, no. 11 (2007): 1332. http://dx.doi.org/10.1182/blood.v110.11.1332.1332.

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Abstract Telomeres are the very ends of chromosomes and protect the genome from recombination, end-to-end-fusion, and recognition as damaged DNA. Telomeres are eroded with each cell division, eventually reaching such critically short length as to cause cell cycle arrest, apoptosis, or genomic instability. In most highly proliferative cells, including hematopoietic stem cells and T lymphocytes, telomere attrition is countered by telomere extension by telomerase reverse transcriptase complex. The majority of cancer cells also express telomerase, which maintains telomere length and allows indefin

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Ogrocká, Anna, Pavla Polanská, Eva Majerová, Zlatko Janeba, Jiří Fajkus, and Miloslava Fojtová. "Compromised telomere maintenance in hypomethylated Arabidopsis thaliana plants." Nucleic Acids Research 42, no. 5 (2013): 2919–31. http://dx.doi.org/10.1093/nar/gkt1285.

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Abstract Telomeres, nucleoprotein structures at the ends of linear eukaryotic chromosomes, are important for the maintenance of genomic stability. Telomeres were considered as typical heterochromatic regions, but in light of recent results, this view should be reconsidered. Asymmetrically located cytosines in plant telomeric DNA repeats may be substrates for a DNA methyltransferase enzyme and indeed, it was shown that these repeats are methylated. Here, we analyse the methylation of telomeric cytosines and the length of telomeres in Arabidopsis thaliana methylation mutants (met 1-3 and ddm 1-8

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Souza, Rhonda F., Tisha Lunsford, Ruben D. Ramirez, et al. "GERD is associated with shortened telomeres in the squamous epithelium of the distal esophagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (2007): G19—G24. http://dx.doi.org/10.1152/ajpgi.00055.2007.

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Telomeres are repetitive DNA sequences located at the ends of chromosomes. Telomeres are shortened by repeated cell divisions and by oxidative DNA damage, and cells with critically shortened telomeres cannot divide. We hypothesized that chronic gastroesophageal reflux disease (GERD)-induced injury of the esophageal squamous epithelium results in progressive telomeric shortening that eventually might interfere with mucosal healing. To address our hypothesis, we compared telomere length and telomerase activity in biopsy specimens of esophageal squamous epithelium from GERD patients and control p

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Blackburn, Elizabeth H., Carol W. Greider, Eric Henderson, Margaret S. Lee, Janis Shampay, and Dorothy Shippen-Lentz. "Recognition and elongation of telomeres by telomerase." Genome 31, no. 2 (1989): 553–60. http://dx.doi.org/10.1139/g89-104.

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Telomeres stabilize chromosomal ends and allow their complete replication in vivo. In diverse eukaryotes, the essential telomeric DNA sequence consists of variable numbers of tandem repeats of simple, G + C rich sequences, with a strong strand bias of G residues on the strand oriented 5′ to 3′ toward the chromosomal terminus. This strand forms a protruding 3′ overhang at the chromosomal terminus in three different eukaryotes analyzed. Analysis of yeast and protozoan telomeres showed that telomeres are dynamic structures in vivo, being acted on by shortening and lengthening activities. We previ

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Bunch, Jeremy T., Nancy S. Bae, Jessica Leonardi, and Peter Baumann. "Distinct Requirements for Pot1 in Limiting Telomere Length and Maintaining Chromosome Stability." Molecular and Cellular Biology 25, no. 13 (2005): 5567–78. http://dx.doi.org/10.1128/mcb.25.13.5567-5578.2005.

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ABSTRACT The fission yeast Pot1 (protection of telomeres) protein binds to the single-stranded extensions at the ends of telomeres, where its presence is critical for the maintenance of linear chromosomes. Homologs of Pot1 have been identified in a wide variety of eukaryotes, including plants, animals, and humans. We now show that Pot1 plays dual roles in telomere length regulation and chromosome end protection. Using a series of Pot1 truncation mutants, we have defined distinct areas of the protein required for chromosome stability and for limiting access to telomere ends by telomerase. We pr

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Lister-Shimauchi, Evan H., Benjamin McCarthy, Michael Lippincott, and Shawn Ahmed. "Genetic and Epigenetic Inheritance at Telomeres." Epigenomes 6, no. 1 (2022): 9. http://dx.doi.org/10.3390/epigenomes6010009.

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Transgenerational inheritance can occur at telomeres in distinct contexts. Deficiency for telomerase or telomere-binding proteins in germ cells can result in shortened or lengthened chromosome termini that are transmitted to progeny. In human families, altered telomere lengths can result in stem cell dysfunction or tumor development. Genetic inheritance of altered telomeres as well as mutations that alter telomeres can result in progressive telomere length changes over multiple generations. Telomeres of yeast can modulate the epigenetic state of subtelomeric genes in a manner that is mitotical

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Liu, Jun, Lihui Wang, Zhiguo Wang, and Jun-Ping Liu. "Roles of Telomere Biology in Cell Senescence, Replicative and Chronological Ageing." Cells 8, no. 1 (2019): 54. http://dx.doi.org/10.3390/cells8010054.

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Telomeres with G-rich repetitive DNA and particular proteins as special heterochromatin structures at the termini of eukaryotic chromosomes are tightly maintained to safeguard genetic integrity and functionality. Telomerase as a specialized reverse transcriptase uses its intrinsic RNA template to lengthen telomeric G-rich strand in yeast and human cells. Cells sense telomere length shortening and respond with cell cycle arrest at a certain size of telomeres referring to the “Hayflick limit.” In addition to regulating the cell replicative senescence, telomere biology plays a fundamental role in

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Martin, Aegina Adams, Isabelle Dionne, Raymund J. Wellinger та Connie Holm. "The Function of DNA Polymerase α at Telomeric G Tails Is Important for Telomere Homeostasis". Molecular and Cellular Biology 20, № 3 (2000): 786–96. http://dx.doi.org/10.1128/mcb.20.3.786-796.2000.

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ABSTRACT Telomere length control is influenced by several factors, including telomerase, the components of telomeric chromatin structure, and the conventional replication machinery. Although known components of the replication machinery can influence telomere length equilibrium, little is known about why mutations in certain replication proteins cause dramatic telomere lengthening. To investigate the cause of telomere elongation in cdc17/pol1 (DNA polymerase α) mutants, we examined telomeric chromatin, as measured by its ability to repress transcription on telomere-proximal genes, and telomeri

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Grandin, Nathalie, and Michel Charbonneau. "Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification." Molecular and Cellular Biology 29, no. 4 (2008): 965–85. http://dx.doi.org/10.1128/mcb.00817-08.

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ABSTRACT In the absence of telomerase, telomeres erode, provoking accumulation of DNA damage and death by senescence. Rare survivors arise, however, due to Rad52-based amplification of telomeric sequences by homologous recombination. The present study reveals that in budding yeast cells, postsenescence survival relying on amplification of the TG1-3 telomeric repeats can take place in the absence of Rad52 when overelongated telomeres are present during senescence (hence its designation ILT, for inherited-long-telomere, pathway). By growth competition, the Rad52-independent pathway was almost as

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Groff-Vindman, Cindy, Anthony J. Cesare, Shobhana Natarajan, Jack D. Griffith, and Michael J. McEachern. "Recombination at Long Mutant Telomeres Produces Tiny Single- and Double-Stranded Telomeric Circles." Molecular and Cellular Biology 25, no. 11 (2005): 4406–12. http://dx.doi.org/10.1128/mcb.25.11.4406-4412.2005.

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ABSTRACT Recombinational telomere elongation (RTE) known as alternate lengthening of telomeres is the mechanism of telomere maintenance in up to 5 to 10% of human cancers. The telomeres of yeast mutants lacking telomerase can also be maintained by recombination. Previously, we proposed the roll-and-spread model to explain this elongation in the yeast Kluveromyces lactis. This model suggests that a very small (∼100-bp) circular molecule of telomeric DNA is copied by a rolling circle event to generate a single long telomere. The sequence of this primary elongated telomere is then spread by recom

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Niida, Hiroyuki, Yoichi Shinkai, M. Prakash Hande, et al. "Telomere Maintenance in Telomerase-Deficient Mouse Embryonic Stem Cells: Characterization of an Amplified Telomeric DNA." Molecular and Cellular Biology 20, no. 11 (2000): 4115–27. http://dx.doi.org/10.1128/mcb.20.11.4115-4127.2000.

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ABSTRACT Telomere dynamics, chromosomal instability, and cellular viability were studied in serial passages of mouse embryonic stem (ES) cells in which the telomerase RNA (mTER) gene was deleted. These cells lack detectable telomerase activity, and their growth rate was reduced after more than 300 divisions and almost zero after 450 cell divisions. After this growth crisis, survivor cells with a rapid growth rate did emerge. Such survivors were found to maintain functional telomeres in a telomerase-independent fashion. Although telomerase-independent telomere maintenance has been reported for

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