Relevant bibliographies by topics / Rif2, Tel1, telomere, yeast

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Rif2, Tel1, telomere, yeast'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Rif2, Tel1, telomere, yeast"

1

Craven, Rolf J., and Thomas D. Petes. "Dependence of the Regulation of Telomere Length on the Type of Subtelomeric Repeat in the Yeast Saccharomyces cerevisiae." Genetics 152, no. 4 (1999): 1531–41. http://dx.doi.org/10.1093/genetics/152.4.1531.

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Abstract In the yeast Saccharomyces cerevisiae, chromosomes terminate with ∼400 bp of a simple repeat poly(TG1-3). Based on the arrangement of subtelomeric X and Y′ repeats, two types of yeast telomeres exist, those with both X and Y′ (Y′ telomeres) and those with only X (X telomeres). Mutations that result in abnormally short or abnormally long poly(TG1-3) tracts have been previously identified. In this study, we investigated telomere length in strains with two classes of mutations, one that resulted in short poly(TG1-3) tracts (tel1) and one that resulted in elongated tracts (pif1, rap1-17,
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2

Viscardi, Valeria, Enrico Baroni, Michele Romano, Giovanna Lucchini, and Maria Pia Longhese. "Sudden Telomere Lengthening Triggers a Rad53-dependent Checkpoint inSaccharomyces cerevisiae." Molecular Biology of the Cell 14, no. 8 (2003): 3126–43. http://dx.doi.org/10.1091/mbc.e02-11-0719.

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Telomeres are specialized functional complexes that ensure chromosome stability by protecting chromosome ends from fusions and degradation and avoiding chromosomal termini from being sensed as DNA breaks. Budding yeast Tel1 is required both for telomere metabolism and for a Rad53-dependent checkpoint responding to unprocessed double-strand breaks. We show that overexpression of a GAL1-TEL1 fusion causes transient telomere lengthening and activation of a Rad53-dependent G2/M checkpoint in cells whose telomeres are short due to the lack of either Tel1 or Yku70. Sudden telomere elongation and che
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3

Fukunaga, Kenzo, Yukinori Hirano, and Katsunori Sugimoto. "Subtelomere-binding protein Tbf1 and telomere-binding protein Rap1 collaborate to inhibit localization of the Mre11 complex to DNA ends in budding yeast." Molecular Biology of the Cell 23, no. 2 (2012): 347–59. http://dx.doi.org/10.1091/mbc.e11-06-0568.

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Chromosome ends, known as telomeres, have to be distinguished from DNA double-strand breaks that activate DNA damage checkpoints. In budding yeast, the Mre11-Rad50-Xrs2 (MRX) complex associates with DNA ends and promotes checkpoint activation. Rap1 binds to double-stranded telomeric regions and recruits Rif1 and Rif2 to telomeres. Rap1 collaborates with Rif1 and Rif2 and inhibits MRX localization to DNA ends. This Rap1-Rif1-Rif2 function becomes attenuated at shortened telomeres. Here we show that Rap1 acts together with the subtelomere-binding protein Tbf1 and inhibits MRX localization to DNA
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4

Sholes, Samantha L., Kayarash Karimian, Ariel Gershman, Thomas J. Kelly, Winston Timp, and Carol W. Greider. "Chromosome-specific telomere lengths and the minimal functional telomere revealed by nanopore sequencing." Genome Research 32, no. 4 (2021): 616–28. http://dx.doi.org/10.1101/gr.275868.121.

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We developed a method to tag telomeres and measure telomere length by nanopore sequencing in the yeast S. cerevisiae. Nanopore allows long-read sequencing through the telomere, through the subtelomere, and into unique chromosomal sequence, enabling assignment of telomere length to a specific chromosome end. We observed chromosome end–specific telomere lengths that were stable over 120 cell divisions. These stable chromosome-specific telomere lengths may be explained by slow clonal variation or may represent a new biological mechanism that maintains equilibrium unique to each chromosome end. We
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5

Ji, Hong, Margaret H. Platts, Latif M. Dharamsi, and Katherine L. Friedman. "Regulation of Telomere Length by an N-Terminal Region of the Yeast Telomerase Reverse Transcriptase." Molecular and Cellular Biology 25, no. 20 (2005): 9103–14. http://dx.doi.org/10.1128/mcb.25.20.9103-9114.2005.

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ABSTRACT Telomerase is a reverse transcriptase that maintains chromosome integrity through synthesis of repetitive telomeric sequences on the ends of eukaryotic chromosomes. In the yeast Saccharomyces cerevisiae, telomere length homeostasis is achieved through negative regulation of telomerase access to the chromosome terminus by telomere-bound Rap1 protein and its binding partners, Rif1p and Rif2p, and positive regulation by factors such as Ku70/80, Tel1p, and Cdc13p. Here we report the identification of mutations within an N-terminal region (region I) of the yeast telomerase catalytic subuni
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6

Zhang, Ling-Li, Zhenfang Wu, and Jin-Qiu Zhou. "Tel1 and Rif2 oppositely regulate telomere protection at uncapped telomeres in Saccharomyces cerevisiae." Journal of Genetics and Genomics 45, no. 9 (2018): 467–76. http://dx.doi.org/10.1016/j.jgg.2018.09.001.

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7

Nakamura, Toru M., Bettina A. Moser, and Paul Russell. "Telomere Binding of Checkpoint Sensor and DNA Repair Proteins Contributes to Maintenance of Functional Fission Yeast Telomeres." Genetics 161, no. 4 (2002): 1437–52. http://dx.doi.org/10.1093/genetics/161.4.1437.

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Abstract Telomeres, the ends of linear chromosomes, are DNA double-strand ends that do not trigger a cell cycle arrest and yet require checkpoint and DNA repair proteins for maintenance. Genetic and biochemical studies in the fission yeast Schizosaccharomyces pombe were undertaken to understand how checkpoint and DNA repair proteins contribute to telomere maintenance. On the basis of telomere lengths of mutant combinations of various checkpoint-related proteins (Rad1, Rad3, Rad9, Rad17, Rad26, Hus1, Crb2, Chk1, Cds1), Tel1, a telomere-binding protein (Taz1), and DNA repair proteins (Ku70, Rad3
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8

Ogi, Hiroo, Greicy H. Goto, Avik Ghosh, Sevil Zencir, Everett Henry, and Katsunori Sugimoto. "Requirement of the FATC domain of protein kinase Tel1 for localization to DNA ends and target protein recognition." Molecular Biology of the Cell 26, no. 19 (2015): 3480–88. http://dx.doi.org/10.1091/mbc.e15-05-0259.

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Two large phosphatidylinositol 3-kinase–related protein kinases (PIKKs), ATM and ATR, play a central role in the DNA damage response pathway. PIKKs contain a highly conserved extreme C-terminus called the FRAP-ATM-TRRAP-C-terminal (FATC) domain. In budding yeast, ATM and ATR correspond to Tel1 and Mec1, respectively. In this study, we characterized functions of the FATC domain of Tel1 by introducing substitution or truncation mutations. One substitution mutation, termed tel1-21, and a truncation mutation, called tel1-ΔC, did not significantly affect the expression level. The tel1-21 mutation i
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9

Craven, Rolf J., Patricia W. Greenwell, Margaret Dominska, and Thomas D. Petes. "Regulation of Genome Stability by TEL1 and MEC1, Yeast Homologs of the Mammalian ATM and ATR Genes." Genetics 161, no. 2 (2002): 493–507. http://dx.doi.org/10.1093/genetics/161.2.493.

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Abstract In eukaryotes, a family of related protein kinases (the ATM family) is involved in regulating cellular responses to DNA damage and telomere length. In the yeast Saccharomyces cerevisiae, two members of this family, TEL1 and MEC1, have functionally redundant roles in both DNA damage repair and telomere length regulation. Strains with mutations in both genes are very sensitive to DNA damaging agents, have very short telomeres, and undergo cellular senescence. We find that strains with the double mutant genotype also have ∼80-fold increased rates of mitotic recombination and chromosome l
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10

Hirano, Yukinori, and Katsunori Sugimoto. "Cdc13 Telomere Capping Decreases Mec1 Association but Does Not Affect Tel1 Association with DNA Ends." Molecular Biology of the Cell 18, no. 6 (2007): 2026–36. http://dx.doi.org/10.1091/mbc.e06-12-1074.

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Chromosome ends, known as telomeres, have to be distinguished from DNA breaks that activate DNA damage checkpoint. Two large protein kinases, ataxia-teleangiectasia mutated (ATM) and ATM-Rad3-related (ATR), control not only checkpoint activation but also telomere length. In budding yeast, Mec1 and Tel1 correspond to ATR and ATM, respectively. Here, we show that Cdc13-dependent telomere capping attenuates Mec1 association with DNA ends. The telomeric TG repeat sequence inhibits DNA degradation and decreases Mec1 accumulation at the DNA end. The TG-mediated degradation block requires binding of
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Dissertations / Theses on the topic "Rif2, Tel1, telomere, yeast"

1

MARTINA, MARINA. "Roles of shelterin-like proteins and yku in saccharomyces cerevisiae telomere homeostasis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41884.

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Telomeres are specialized nucleoprotein complexes that distinguish the natural ends of linear chromosomes from intrachromosomal double-strand breaks. In fact, telomeres are protected from DNA damage checkpoints, homologous recombination or end-to-end fusions that normally promote repair of intrachromosomal DNA breaks. When chromosome end protection fails, dysfunctional telomeres are targeted by the DNA repair and recombination apparatus, whose outcomes range from the generation of chromosomal abnormalities, general hallmarks for human cancer cells, to permanent cell cycle arrest and cell death
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ANBALAGAN, SAVANI. "Role of saccharomyces cerevisiae Rif1 and Rif2 proteins in protection of telomeres." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43717.

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Eukaryotic cells distinguish their chromosome ends from accidental DNA double-strand breaks (DSBs) by packaging them into protective structures called telomeres that prevent DNA repair/recombination activities. In this work, we investigated the role of key telomeric proteins in protecting Saccharomyces cerevisiae telomeres from degradation. We show that the shelterin-like proteins Rif1, Rif2, and Rap1 inhibit nucleolytic processing at both de novo and native telomeres during G1 and G2 cell cycle phases, with Rif2 and Rap1 showing the strongest effects. Also Yku prevents telomere resection in G
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