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Статті в журналах з теми "Telomeres And Telomerase Biology"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 31 липня 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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2

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

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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4

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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Анотація:

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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5

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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6

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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7

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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8

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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Анотація:

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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9

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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Анотація:

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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10

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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11

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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12

Zhou, Jianlong, Kyoko Hidaka, and Bruce Futcher. "The Est1 Subunit of Yeast Telomerase Binds the Tlc1 Telomerase RNA." Molecular and Cellular Biology 20, no. 6 (2000): 1947–55. http://dx.doi.org/10.1128/mcb.20.6.1947-1955.2000.

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ABSTRACT Est1 is a component of yeast telomerase, and est1mutants have senescence and telomere loss phenotypes. The exact function of Est1 is not known, and it is not homologous to components of other telomerases. We previously showed that Est1 protein coimmunoprecipitates with Tlc1 (the telomerase RNA) as well as with telomerase activity. Est1 has homology to Ebs1, an uncharacterized yeast open reading frame product, including homology to a putative RNA recognition motif (RRM) of Ebs1. Deletion of EBS1 results in short telomeres. We created point mutations in a putative RRM of Est1. One mutan

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13

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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14

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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Анотація:

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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15

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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16

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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17

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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18

Ray, Alo, and Kurt W. Runge. "The C Terminus of the Major Yeast Telomere Binding Protein Rap1p Enhances Telomere Formation." Molecular and Cellular Biology 18, no. 3 (1998): 1284–95. http://dx.doi.org/10.1128/mcb.18.3.1284.

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ABSTRACT The telomeres of most organisms consist of short repeated sequences that can be elongated by telomerase, a reverse transcriptase complex that contains its own RNA template for the synthesis of telomere repeats. In Saccharomyces cerevisiae, the RAP1gene encodes the major telomere binding protein Rap1p. Here we use a quantitative telomere formation assay to demonstrate that Rap1p C termini can enhance telomere formation more than 30-fold when they are located at internal sites. This stimulation is distinct from protection from degradation. Enhancement of formation required the gene for

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19

Watson, J. Matthew, and Dorothy E. Shippen. "Telomere Rapid Deletion Regulates Telomere Length in Arabidopsis thaliana." Molecular and Cellular Biology 27, no. 5 (2006): 1706–15. http://dx.doi.org/10.1128/mcb.02059-06.

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ABSTRACT Telomere length is maintained in species-specific equilibrium primarily through a competition between telomerase-mediated elongation and the loss of terminal DNA through the end-replication problem. Recombinational activities are also capable of both lengthening and shortening telomeres. Here we demonstrate that elongated telomeres in Arabidopsis Ku70 mutants reach a new length set point after three generations. Restoration of wild-type Ku70 in these mutants leads to discrete telomere-shortening events consistent with telomere rapid deletion (TRD). These findings imply that the longer

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20

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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21

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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22

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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23

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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24

Lansdorp, Peter M. "Telomeres, stem cells, and hematology." Blood 111, no. 4 (2008): 1759–66. http://dx.doi.org/10.1182/blood-2007-09-084913.

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Telomeres are highly dynamic structures that adjust the cellular response to stress and growth stimulation based on previous cell divisions. This critical function is accomplished by progressive telomere shortening and DNA damage responses activated by chromosome ends without sufficient telomere repeats. Repair of critically short telomeres by telomerase or recombination is limited in most somatic cells, and apoptosis or cellular senescence is triggered when too many uncapped telomeres accumulate. The chance of the latter increases as the average telomere length decreases. The average telomere

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25

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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26

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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27

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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28

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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29

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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30

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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31

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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Veverka, Janovič, and Hofr. "Quantitative Biology of Human Shelterin and Telomerase: Searching for the Weakest Point." International Journal of Molecular Sciences 20, no. 13 (2019): 3186. http://dx.doi.org/10.3390/ijms20133186.

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The repetitive telomeric DNA at chromosome ends is protected from unwanted repair by telomere-associated proteins, which form the shelterin complex in mammals. Recent works have provided new insights into the mechanisms of how human shelterin assembles and recruits telomerase to telomeres. Inhibition of telomerase activity and telomerase recruitment to chromosome ends is a promising target for anticancer therapy. Here, we summarize results of quantitative assessments and newly emerged structural information along with the status of the most promising approaches to telomerase inhibition in canc

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33

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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34

Meier, Bettina, Lucia Driller, Sigrun Jaklin, and Heidi M. Feldmann. "New Function of CDC13 in Positive Telomere Length Regulation." Molecular and Cellular Biology 21, no. 13 (2001): 4233–45. http://dx.doi.org/10.1128/mcb.21.13.4233-4245.2001.

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ABSTRACT Two roles for the Saccharomyces cerevisiae Cdc13 protein at the telomere have previously been characterized: it recruits telomerase to the telomere and protects chromosome ends from degradation. In a synthetic lethality screen with YKU70, the 70-kDa subunit of the telomere-associated Yku heterodimer, we identified a new mutation in CDC13, cdc13-4, that points toward an additional regulatory function of CDC13. AlthoughCDC13 is an essential telomerase component in vivo, no replicative senescence can be observed in cdc13-4 cells. Telomeres of cdc13-4 mutants shorten for about 150 generat

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35

Rembiałkowska, Nina, Mikołaj Sędzik, Monika Kisielewska, et al. "Telomere Maintenance and DNA Repair: A Bidirectional Relationship in Cancer Biology and Therapy." Cancers 17, no. 14 (2025): 2284. https://doi.org/10.3390/cancers17142284.

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Telomeres are repetitive DNA sequences at the ends of chromosomes that protect against genomic instability and prevent unwanted DNA damage responses. In most somatic cells, telomeres progressively shorten with each division, limiting cellular lifespan. However, cancer cells bypass this limitation by activating telomerase or the alternative lengthening of telomeres, enabling unchecked proliferation and tumor progression. This review examines the molecular mechanisms underlying telomere maintenance and their intricate relationship with DNA repair pathways. We discuss how telomere-associated prot

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36

Counter, CM, J. Gupta, CB Harley, B. Leber, and S. Bacchetti. "Telomerase activity in normal leukocytes and in hematologic malignancies." Blood 85, no. 9 (1995): 2315–20. http://dx.doi.org/10.1182/blood.v85.9.2315.bloodjournal8592315.

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Telomeres are essential for function and stability of eukaryotic chromosomes. In the absence of telomerase, the enzyme that synthesizes telomeric DNA, telomeres shorten with cell division, a process thought to contribute to cell senescence and the proliferative crisis of transformed cells. We reported telomere stabilization concomitant with detection of telomerase activity in cells immortalized in vitro and in ovarian carcinoma cells, and suggested that telomerase is essential for unlimited cell proliferation. We have now examined the temporal pattern of telomerase expression in selected hemat

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37

Ancelin, Katia, Michele Brunori, Serge Bauwens, et al. "Targeting Assay To Study the cis Functions of Human Telomeric Proteins: Evidence for Inhibition of Telomerase by TRF1 and for Activation of Telomere Degradation by TRF2." Molecular and Cellular Biology 22, no. 10 (2002): 3474–87. http://dx.doi.org/10.1128/mcb.22.10.3474-3487.2002.

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ABSTRACT We investigated the control of telomere length by the human telomeric proteins TRF1 and TRF2. To this end, we established telomerase-positive cell lines in which the targeting of these telomeric proteins to specific telomeres could be induced. We demonstrate that their targeting leads to telomere shortening. This indicates that these proteins act in cis to repress telomere elongation. Inhibition of telomerase activity by a modified oligonucleotide did not further increase the pace of telomere erosion caused by TRF1 targeting, suggesting that telomerase itself is the target of TRF1 reg

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38

Fajkus, J., M. Šimíčková, and J. Maláska. "Tiptoeing to chromosome tips: facts, promises and perils of today's human telomere biology." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 357, no. 1420 (2002): 545–62. http://dx.doi.org/10.1098/rstb.2001.1053.

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The past decade has witnessed an explosion of knowledge concerning the structure and function of chromosome terminal structures—telomeres. Today's telomere research has advanced from a pure descriptive approach of DNA and protein components to an elementary understanding of telomere metabolism, and now to promising applications in medicine. These applications include ‘passive’ ones, among which the use of analysis of telomeres and telomerase (a cellular reverse transcriptase that synthesizes telomeres) for cancer diagnostics is the best known. The ‘active’ applications involve targeted downreg

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Osterhage, Jennifer L., and Katherine L. Friedman. "Chromosome End Maintenance by Telomerase." Journal of Biological Chemistry 284, no. 24 (2009): 16061–65. http://dx.doi.org/10.1074/jbc.r900011200.

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Telomeres, protein-DNA complexes at the ends of eukaryotic linear chromosomes, are essential for genome stability. The accumulation of chromosomal abnormalities in the absence of proper telomere function is implicated in human aging and cancer. Repetitive telomeric sequences are maintained by telomerase, a ribonucleoprotein complex containing a reverse transcriptase subunit, a template RNA, and accessory components. Telomere elongation is regulated at multiple levels, including assembly of the telomerase holoenzyme, recruitment of telomerase to the chromosome terminus, and telomere accessibili

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Criscuolo, F., S. Smith, S. Zahn, B. J. Heidinger, and M. F. Haussmann. "Experimental manipulation of telomere length: does it reveal a corner-stone role for telomerase in the natural variability of individual fitness?" Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1741 (2018): 20160440. http://dx.doi.org/10.1098/rstb.2016.0440.

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Telomeres, the non-coding ends of linear chromosomes, are thought to be an important mechanism of individual variability in performance. Research suggests that longer telomeres are indicative of better health and increased fitness; however, many of these data are correlational and whether these effects are causal are poorly understood. Experimental tests are emerging in medical and laboratory-based studies, but these types of experiments are rare in natural populations, which precludes conclusions at an evolutionary level. At the crossroads between telomere length and fitness is telomerase, an

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Armbruster, Blaine N., Katherine T. Etheridge, Dominique Broccoli, and Christopher M. Counter. "Putative Telomere-Recruiting Domain in the Catalytic Subunit of Human Telomerase." Molecular and Cellular Biology 23, no. 9 (2003): 3237–46. http://dx.doi.org/10.1128/mcb.23.9.3237-3246.2003.

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ABSTRACT Telomerase, the enzyme that elongates telomeres, is essential to maintain telomere length and to immortalize most cancer cells. However, little is known about the regulation of this enzyme in higher eukaryotes. We previously described a domain in the hTERT telomerase catalytic subunit that is essential for telomere elongation and cell immortalization in vivo but dispensable for catalytic activity in vitro. Here, we show that fusions of hTERT containing different mutations in this domain to the telomere binding protein hTRF2 redirected the mutated hTERT to telomeres and rescued its in

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42

McNees, Carolyn J., Agueda M. Tejera, Paula Martínez, et al. "ATR suppresses telomere fragility and recombination but is dispensable for elongation of short telomeres by telomerase." Journal of Cell Biology 188, no. 5 (2010): 639–52. http://dx.doi.org/10.1083/jcb.200908136.

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Telomere shortening caused by incomplete DNA replication is balanced by telomerase-mediated telomere extension, with evidence indicating that the shortest telomeres are preferred substrates in primary cells. Critically short telomeres are detected by the cellular DNA damage response (DDR) system. In budding yeast, the important DDR kinase Tel1 (homologue of ATM [ataxia telangiectasia mutated]) is vital for telomerase recruitment to short telomeres, but mammalian ATM is dispensable for this function. We asked whether closely related ATR (ATM and Rad3 related) kinase, which is important for prev

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Perrem, Kilian, Lorel M. Colgin, Axel A. Neumann, Thomas R. Yeager, and Roger R. Reddel. "Coexistence of Alternative Lengthening of Telomeres and Telomerase in hTERT-Transfected GM847 Cells." Molecular and Cellular Biology 21, no. 12 (2001): 3862–75. http://dx.doi.org/10.1128/mcb.21.12.3862-3875.2001.

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ABSTRACT It has been shown previously that some immortalized human cells maintain their telomeres in the absence of significant levels of telomerase activity by a mechanism referred to as alternative lengthening of telomeres (ALT). Cells utilizing ALT have telomeres of very heterogeneous length, ranging from very short to very long. Here we report the effect of telomerase expression in the ALT cell line GM847. Expression of exogenous hTERT in GM847 (GM847/hTERT) cells resulted in lengthening of the shortest telomeres; this is the first evidence that expression of hTERT in ALT cells can induce

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44

Dahlén, Maria, Per Sunnerhagen, and Teresa S. F. Wang. "Replication Proteins Influence the Maintenance of Telomere Length and Telomerase Protein Stability." Molecular and Cellular Biology 23, no. 9 (2003): 3031–42. http://dx.doi.org/10.1128/mcb.23.9.3031-3042.2003.

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ABSTRACT We investigated the effects of fission yeast replication genes on telomere length maintenance and identified 20 mutant alleles that confer lengthening or shortening of telomeres. The telomere elongation was telomerase dependent in the replication mutants analyzed. Furthermore, the telomerase catalytic subunit, Trt1, and the principal initiation and lagging-strand synthesis DNA polymerase, Polα, were reciprocally coimmunoprecipitated, indicating these proteins physically coexist as a complex in vivo. In a polα mutant that exhibited abnormal telomere lengthening and slightly reduced tel

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Roeth, Alexander, Jan Duerig, Heike Himmelreich, et al. "T-Cells with Extremely Short Telomeres and High Telomerase Activity in T-Cell Prolymphocytic Leukemia (T-PLL): The Ideal Target for Telomerase Inhibition." Blood 108, no. 11 (2006): 497. http://dx.doi.org/10.1182/blood.v108.11.497.497.

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Abstract T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoproliferative disease characterized by the expansion of a T-cell clone derived from immuno-competent post-thymic T-lymphocytes. Important mechanisms involved in expansion of human malignant cells are reactivation of telomerase, an enzyme complex, which is able to compensate the loss of telomere repeats by cell division, and maintenance or elongation of telomere length. To investigate the role of telomeres and telomerase we measured telomere length by automated multicolor flow-FISH and telomerase activity by telomeric re

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46

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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Underwood, Dana H., Robert P. Zinzen, and Michael J. McEachern. "Template Requirements for Telomerase Translocation in Kluyveromyces lactis." Molecular and Cellular Biology 24, no. 2 (2004): 912–23. http://dx.doi.org/10.1128/mcb.24.2.912-923.2004.

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ABSTRACT Telomeres are synthesized by telomerase, a specialized reverse transcriptase, which contains a template in its intrinsic RNA component. In Kluyveromyces lactis, the repeats synthesized by the wild-type telomerase are 25 nucleotides (nt) in length and uniform in sequence. To determine the role of the 5-nt repeats defining the ends of the K. lactis telomerase RNA template in telomerase translocation, we have made mutations in and around them and observed their effects on telomere length and the sequence of newly made telomeric repeats. These template mutations typically result in telome

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Cong, Yu-Sheng, Woodring E. Wright, and Jerry W. Shay. "Human Telomerase and Its Regulation." Microbiology and Molecular Biology Reviews 66, no. 3 (2002): 407–25. http://dx.doi.org/10.1128/mmbr.66.3.407-425.2002.

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SUMMARY The telomere is a special functional complex at the end of linear eukaryotic chromosomes, consisting of tandem repeat DNA sequences and associated proteins. It is essential for maintaining the integrity and stability of linear eukaryotic genomes. Telomere length regulation and maintenance contribute to normal human cellular aging and human diseases. The synthesis of telomeres is mainly achieved by the cellular reverse transcriptase telomerase, an RNA-dependent DNA polymerase that adds telomeric DNA to telomeres. Expression of telomerase is usually required for cell immortalization and

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Aubert, Geraldine, and Peter M. Lansdorp. "Telomeres and Aging." Physiological Reviews 88, no. 2 (2008): 557–79. http://dx.doi.org/10.1152/physrev.00026.2007.

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Telomeres play a central role in cell fate and aging by adjusting the cellular response to stress and growth stimulation on the basis of previous cell divisions and DNA damage. At least a few hundred nucleotides of telomere repeats must “cap” each chromosome end to avoid activation of DNA repair pathways. Repair of critically short or “uncapped” telomeres by telomerase or recombination is limited in most somatic cells and apoptosis or cellular senescence is triggered when too many “uncapped” telomeres accumulate. The chance of the latter increases as the average telomere length decreases. The

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Hoh, Yin Kiong. "An Instant Update on Telomeres and Telomerase." American Biology Teacher 79, no. 8 (2017): 615–20. http://dx.doi.org/10.1525/abt.2017.79.8.615.

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The DNA sequence of Tetrahymena telomeres was the first to be determined among all telomeres by Elizabeth Blackburn and Joseph Gall in 1978. In 1982, Jack Szostak and Blackburn showed that the unique DNA sequence contained in the telomeres served to protect the chromosomes from degradation. In 1985, Carol Greider and Blackburn showed how the telomeres could be elongated by the enzyme telomerase. These discoveries are milestones marking the start of the molecular era of telomere biology. Telomeres occur at the ends of chromosomes, like the plastic sheaths at the ends of shoelaces. The significa

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