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Articles de revues sur le sujet « Rif2, Tel1, telomere, yeast »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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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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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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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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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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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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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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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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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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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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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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Fritz, Eberhard, Anna A. Friedl, Ralf M. Zwacka, Friederike Eckardt-Schupp, and M. Stephen Meyn. "The YeastTEL1Gene Partially Substitutes for HumanATMin Suppressing Hyperrecombination, Radiation-Induced Apoptosis and Telomere Shortening in A-T Cells." Molecular Biology of the Cell 11, no. 8 (2000): 2605–16. http://dx.doi.org/10.1091/mbc.11.8.2605.

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Homozygous mutations in the human ATM gene lead to a pleiotropic clinical phenotype of ataxia-telangiectasia (A-T) patients and correlating cellular deficiencies in cells derived from A-T donors. Saccharomyces cerevisiae tel1 mutants lacking Tel1p, which is the closest sequence homologue to the ATM protein, share some of the cellular defects with A-T. Through genetic complementation of A-T cells with the yeast TEL1 gene, we provide evidence that Tel1p can partially compensate for ATM in suppressing hyperrecombination, radiation-induced apoptosis, and telomere shortening. Complementation appear

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12

Ritchie, Kim B., Julia C. Mallory, and Thomas D. Petes. "Interactions of TLC1 (Which Encodes the RNA Subunit of Telomerase), TEL1, and MEC1 in Regulating Telomere Length in the Yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 19, no. 9 (1999): 6065–75. http://dx.doi.org/10.1128/mcb.19.9.6065.

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ABSTRACT In the yeast Saccharomyces cerevisiae, chromosomes terminate with a repetitive sequence [poly(TG1–3)] 350 to 500 bp in length. Strains with a mutation of TEL1, a homolog of the human gene (ATM) mutated in patients with ataxia telangiectasia, have short but stable telomeric repeats. Mutations of TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats. We show tha

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Ritchie, Kim B., and Thomas D. Petes. "The Mre11p/Rad50p/Xrs2p Complex and the Tel1p Function in a Single Pathway for Telomere Maintenance in Yeast." Genetics 155, no. 1 (2000): 475–79. http://dx.doi.org/10.1093/genetics/155.1.475.

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Abstract The Mre11p/Rad50p/Xrs2p complex is involved in the repair of double-strand DNA breaks, nonhomologous end joining, and telomere length regulation. TEL1 is primarily involved in telomere length regulation. By an epistasis analysis, we conclude that Tel1p and the Mre11p/Rad50p/Xrs2p complex function in a single pathway of telomere length regulation.

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Subramanian, Lakxmi, Bettina A. Moser, and Toru M. Nakamura. "Recombination-Based Telomere Maintenance Is Dependent on Tel1-MRN and Rap1 and Inhibited by Telomerase, Taz1, and Ku in Fission Yeast." Molecular and Cellular Biology 28, no. 5 (2007): 1443–55. http://dx.doi.org/10.1128/mcb.01614-07.

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ABSTRACT Fission yeast cells survive loss of the telomerase catalytic subunit Trt1 (TERT) through recombination-based telomere maintenance or through chromosome circularization. Although trt1Δ survivors with linear chromosomes can be obtained, they often spontaneously circularize their chromosomes. Therefore, it was difficult to establish genetic requirements for telomerase-independent telomere maintenance. In contrast, when the telomere-binding protein Taz1 is also deleted, taz1Δ trt1Δ cells are able to stably maintain telomeres. Thus, taz1Δ trt1Δ cells can serve as a valuable tool in underst

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15

Galli, Michela, Chiara Frigerio, Maria Pia Longhese, and Michela Clerici. "The regulation of the DNA damage response at telomeres: focus on kinases." Biochemical Society Transactions 49, no. 2 (2021): 933–43. http://dx.doi.org/10.1042/bst20200856.

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The natural ends of linear chromosomes resemble those of accidental double-strand breaks (DSBs). DSBs induce a multifaceted cellular response that promotes the repair of lesions and slows down cell cycle progression. This response is not elicited at chromosome ends, which are organized in nucleoprotein structures called telomeres. Besides counteracting DSB response through specialized telomere-binding proteins, telomeres also prevent chromosome shortening. Despite of the different fate of telomeres and DSBs, many proteins involved in the DSB response also localize at telomeres and participate

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Poschke, Heiko, Martina Dees, Michael Chang, et al. "Rif2 Promotes a Telomere Fold-Back Structure through Rpd3L Recruitment in Budding Yeast." PLoS Genetics 8, no. 9 (2012): e1002960. http://dx.doi.org/10.1371/journal.pgen.1002960.

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17

Runge, K. W., and V. A. Zakian. "TEL2, an essential gene required for telomere length regulation and telomere position effect in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 6 (1996): 3094–105. http://dx.doi.org/10.1128/mcb.16.6.3094.

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The DNA-protein complexes at the ends of linear eukaryotic chromosomes are called the telomeres. In Saccharomyces cerevisiae, telomeric DNA consists of a variable length of the short repeated sequence C1-3A. The length of yeast telomeres can be altered by mutation, by changing the levels of telomere binding proteins, or by increasing the amount of C1-3A DNA sequences. Cells bearing the tel1-1 or tel2-1 mutations, known previously to have short telomeres, did not respond to perturbations that caused telomere lengthening in wild-type cells. The transcription of genes placed near yeast telomeres

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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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Tsai, Yun-Luen, Shun-Fu Tseng, Shih-Husan Chang, Chuan-Chuan Lin, and Shu-Chun Teng. "Involvement of Replicative Polymerases, Tel1p, Mec1p, Cdc13p, and the Ku Complex in Telomere-Telomere Recombination." Molecular and Cellular Biology 22, no. 16 (2002): 5679–87. http://dx.doi.org/10.1128/mcb.22.16.5679-5687.2002.

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ABSTRACT Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of the reverse transcriptase telomerase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Genetic studies have led to the identification of DNA polymerases, cell cycle checkpoint proteins, and telomere binding proteins involved in the telomerase pathway. However, how these proteins affect telomere-telomere recombination has not been identified to date. Using an assay to trace the in vivo recombinational p

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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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Hailemariam, Sarem, Paolo De Bona, Roberto Galletto, Marcel Hohl, John H. Petrini, and Peter M. Burgers. "The telomere-binding protein Rif2 and ATP-bound Rad50 have opposing roles in the activation of yeast Tel1ATM kinase." Journal of Biological Chemistry 294, no. 49 (2019): 18846–52. http://dx.doi.org/10.1074/jbc.ra119.011077.

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Pennaneach, Vincent, and Richard D. Kolodner. "Recombination and the Tel1 and Mec1 checkpoints differentially effect genome rearrangements driven by telomere dysfunction in yeast." Nature Genetics 36, no. 6 (2004): 612–17. http://dx.doi.org/10.1038/ng1359.

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Pobiega, Sabrina, Olivier Alibert, and Stéphane Marcand. "A new assay capturing chromosome fusions shows a protection trade-off at telomeres and NHEJ vulnerability to low-density ionizing radiation." Nucleic Acids Research 49, no. 12 (2021): 6817–31. http://dx.doi.org/10.1093/nar/gkab502.

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Abstract Chromosome fusions threaten genome integrity and promote cancer by engaging catastrophic mutational processes, namely chromosome breakage–fusion–bridge cycles and chromothripsis. Chromosome fusions are frequent in cells incurring telomere dysfunctions or those exposed to DNA breakage. Their occurrence and therefore their contribution to genome instability in unchallenged cells is unknown. To address this issue, we constructed a genetic assay able to capture and quantify rare chromosome fusions in budding yeast. This chromosome fusion capture (CFC) assay relies on the controlled inacti

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Pizzul, Paolo, Erika Casari, Carlo Rinaldi, et al. "Rif2 interaction with Rad50 counteracts Tel1 functions in checkpoint signalling and DNA tethering by releasing Tel1 from MRX binding." Nucleic Acids Research, January 5, 2024. http://dx.doi.org/10.1093/nar/gkad1246.

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Abstract The yeast Rif2 protein is known to inhibit Mre11 nuclease and the activation of Tel1 kinase through a short motif termed MIN, which binds the Rad50 subunit and simulates its ATPase activity in vitro. The mechanism by which Rif2 restrains Tel1 activation and the consequences of this inhibition at DNA double-strand breaks (DSBs) are poorly understood. In this study, we employed AlphaFold-Multimer modelling to pinpoint and validate the interaction surface between Rif2 MIN and Rad50. We also engineered the rif2-S6E mutation that enhances the inhibitory effect of Rif2 by increasing Rif2-Ra

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Khayat, Freddy, Elda Cannavo, Majedh Alshmery, et al. "Inhibition of MRN activity by a telomere protein motif." Nature Communications 12, no. 1 (2021). http://dx.doi.org/10.1038/s41467-021-24047-2.

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AbstractThe MRN complex (MRX in Saccharomyces cerevisiae, made of Mre11, Rad50 and Nbs1/Xrs2) initiates double-stranded DNA break repair and activates the Tel1/ATM kinase in the DNA damage response. Telomeres counter both outcomes at chromosome ends, partly by keeping MRN-ATM in check. We show that MRX is disabled by telomeric protein Rif2 through an N-terminal motif (MIN, MRN/X-inhibitory motif). MIN executes suppression of Tel1, DNA end-resection and non-homologous end joining by binding the Rad50 N-terminal region. Our data suggest that MIN promotes a transition within MRX that is not condu

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Rosas Bringas, Fernando Rodrigo, Sonia Stinus, Pien de Zoeten, Marita Cohn, and Michael Chang. "Rif2 protects Rap1-depleted telomeres from MRX-mediated degradation in Saccharomyces cerevisiae." eLife 11 (January 19, 2022). http://dx.doi.org/10.7554/elife.74090.

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Rap1 is the main protein that binds double-stranded telomeric DNA in Saccharomyces cerevisiae. Examination of the telomere functions of Rap1 is complicated by the fact that it also acts as a transcriptional regulator of hundreds of genes and is encoded by an essential gene. In this study, we disrupt Rap1 telomere association by expressing a mutant telomerase RNA subunit (tlc1-tm) that introduces mutant telomeric repeats. tlc1-tm cells grow similar to wild-type cells, although depletion of Rap1 at telomeres causes defects in telomere length regulation and telomere capping. Rif2 is a protein nor

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Hass, Evan P., and David C. Zappulla. "The Ku subunit of telomerase binds Sir4 to recruit telomerase to lengthen telomeres in S. cerevisiae." eLife 4 (July 28, 2015). http://dx.doi.org/10.7554/elife.07750.

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In Saccharomyces cerevisiae and in humans, the telomerase RNA subunit is bound by Ku, a ring-shaped protein heterodimer best known for its function in DNA repair. Ku binding to yeast telomerase RNA promotes telomere lengthening and telomerase recruitment to telomeres, but how this is achieved remains unknown. Using telomere-length analysis and chromatin immunoprecipitation, we show that Sir4 – a previously identified Ku-binding protein that is a component of telomeric silent chromatin – is required for Ku-mediated telomere lengthening and telomerase recruitment. We also find that specifically

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Holland, Cory L., Brian A. Sanderson, James K. Titus, et al. "Suppression of telomere capping defects of Saccharomyces cerevisiae yku70 and yku80 mutants by telomerase." G3 Genes|Genomes|Genetics 11, no. 12 (2021). http://dx.doi.org/10.1093/g3journal/jkab359.

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Abstract The Ku complex performs multiple functions inside eukaryotic cells, including protection of chromosomal DNA ends from degradation and fusion events, recruitment of telomerase, and repair of double-strand breaks (DSBs). Inactivation of Ku complex genes YKU70 or YKU80 in cells of the yeast Saccharomyces cerevisiae gives rise to mutants that exhibit shortened telomeres and temperature-sensitive growth. In this study, we have investigated the mechanism by which overexpression of telomerase suppresses the temperature sensitivity of yku mutants. Viability of yku cells was restored by overex

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