Academic literature on the topic 'Telomere Position Effect'
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Journal articles on the topic "Telomere Position Effect":
1
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 (May 1, 2003): 3031–42. http://dx.doi.org/10.1128/mcb.23.9.3031-3042.2003.
Abstract:
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 telomere position effect, the cellular level of the Trt1 protein was significantly lower and the coimmunoprecipitation of Trt1 and Polα was severely compromised compared to those in the wild-type polα cells. Interestingly, ectopic expression of wild-type polα in this polα mutant restored the cellular Trt1 protein to the wild-type level and shortened the telomeres to near-wild-type length. These results suggest that there is a close physical relationship between the replication and telomerase complexes. Thus, mutation of a component of the replication complex can affect the telomeric complex in maintaining both telomere length equilibrium and telomerase protein stability.
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de Bruin, Derik, Sara M. Kantrow, Rachel A. Liberatore, and Virginia A. Zakian. "Telomere Folding Is Required for the Stable Maintenance of Telomere Position Effects in Yeast." Molecular and Cellular Biology 20, no. 21 (November 1, 2000): 7991–8000. http://dx.doi.org/10.1128/mcb.20.21.7991-8000.2000.
Abstract:
ABSTRACT Yeast telomeres reversibly repress the transcription of adjacent genes, a phenomenon called telomere position effect (TPE). TPE is thought to result from Rap1 and Sir protein-mediated spreading of heterochromatin-like structures from the telomeric DNA inwards. Because Rap1p is associated with subtelomeric chromatin as well as with telomeric DNA, yeast telomeres are proposed to form fold-back or looped structures. TPE can be eliminated in trans by deletingSIR genes or in cis by transcribing through the C1–3A/TG1–3 tract of a telomere. We show that the promoter of a telomere-linked URA3 gene was inaccessible to restriction enzymes and that accessibility increased both in a sir3 strain and upon telomere transcription. We also show that subtelomeric chromatin was hypoacetylated at histone H3 and at each of the four acetylatable lysines in histone H4 and that histone acetylation increased both in a sir3 strain and when the telomere was transcribed. When transcription through the telomeric tract occurred in G1-arrested cells, TPE was lost, demonstrating that activation of a silenced telomeric gene can occur in the absence of DNA replication. The loss of TPE that accompanied telomere transcription resulted in the rapid and efficient loss of subtelomeric Rap1p. We propose that telomere transcription disrupts core heterochromatin by eliminating Rap1p-mediated telomere looping. This interpretation suggests that telomere looping is critical for maintaining TPE.
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Park, Yangsuk, and Arthur J. Lustig. "Telomere Structure Regulates the Heritability of Repressed Subtelomeric Chromatin in Saccharomyces cerevisiae." Genetics 154, no. 2 (February 1, 2000): 587–98. http://dx.doi.org/10.1093/genetics/154.2.587.
Abstract:
Abstract Telomeres, the protein-DNA structures present at the termini of linear chromosomes, are capable of conferring a reversible repression of Pol II- and Pol III-transcribed genes positioned in adjacent subtelomeric regions. This phenomenon, termed telomeric silencing, is likely to be the consequence of a more global telomere position effect at the level of chromatin structure. To understand the role of telomere structure in this position effect, we have developed an assay to distinguish between the heritability of transcriptionally repressed and derepressed states in yeast. We have previously demonstrated that an elongated telomeric tract leads to hyperrepression of telomere-adjacent genes. We show here that the predominant effect of elongated telomeres is to increase the inheritance of the repressed state in cis. Interestingly, the presence of elongated telomeres overcomes the partial requirement of yCAF-1 in silencing. We propose that the formation of a specific telomeric structure is necessary for the heritability of repressed subtelomeric chromatin.
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Yu, Eun Young, Olga Steinberg-Neifach, Alain T. Dandjinou, Frances Kang, Ashby J. Morrison, Xuetong Shen, and Neal F. Lue. "Regulation of Telomere Structure and Functions by Subunits of the INO80 Chromatin Remodeling Complex." Molecular and Cellular Biology 27, no. 16 (June 11, 2007): 5639–49. http://dx.doi.org/10.1128/mcb.00418-07.
Abstract:
ABSTRACT ATP-dependent chromatin remodeling complexes have been implicated in the regulation of transcription, replication, and more recently DNA double-strand break repair. Here we report that the Ies3p subunit of the Saccharomyces cerevisiae INO80 chromatin remodeling complex interacts with a conserved tetratricopeptide repeat domain of the telomerase protein Est1p. Deletion of IES3 and some other subunits of the complex induced telomere elongation and altered telomere position effect. In telomerase-negative mutants, loss of Ies3p delayed the emergence of recombinational survivors and stimulated the formation of extrachromosomal telomeric circles in survivors. Deletion of IES3 also resulted in heightened levels of telomere-telomere fusions in telomerase-deficient strains. In addition, a delay in survivor formation was observed in an Arp8p-deficient mutant. Because Arp8p is required for the chromatin remodeling activity of the INO80 complex, the complex may promote recombinational telomere maintenance by altering chromatin structure. Consistent with this notion, we observed preferential localization of multiple subunits of the INO80 complex to telomeres. Our results reveal novel functions for a subunit of the telomerase complex and the INO80 chromatin remodeling complex.
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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 (June 1996): 3094–105. http://dx.doi.org/10.1128/mcb.16.6.3094.
Abstract:
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 is reversibly repressed, a phenomenon called the telomere position effect. The tel2-1 mutation reduced the position effect but did not affect transcriptional repression at the silent mating type cassettes, HMRa and HML alpha. The TEL2 gene was cloned, sequenced, and disrupted. Cells lacking TEL2 function died, with some cells arresting as large cells with three or four small protrusions or "blebs."
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Mason, James M., Alexander Y. Konev, Mikhail D. Golubovsky, and Harald Biessmann. "Cis- andtrans-acting Influences on Telomeric Position Effect inDrosophila melanogasterDetected With a Subterminal Transgene." Genetics 163, no. 3 (March 1, 2003): 917–30. http://dx.doi.org/10.1093/genetics/163.3.917.
Abstract:
AbstractOne model of telomeric position effect (TPE) in Drosophila melanogaster proposes that reporter genes in the vicinity of telomeres are repressed by subterminal telomere-associated sequences (TAS) and that variegation of these genes is the result of competition between the repressive effects of TAS and the stimulating effects of promoters in the terminal HeT-A transposon array. The data presented here support this model, but also suggest that TPE is more complex. Activity of a telomeric white reporter gene increases in response to deletion of some or all of the TAS on the homolog. Only transgenes next to fairly long HeT-A arrays respond to this trans-interaction. HeT-A arrays of 6-18 kb respond by increasing the number of dark spots on the eye, while longer arrays increase the background eye color or increase the number of spots sufficiently to cause them to merge. Thus, expression of a subtelomeric reporter gene is influenced by the telomere structure in cis and trans. We propose that the forces involved in telomere length regulation in Drosophila are the underlying forces that manifest themselves as TPE. In the wild-type telomere TAS may play an important role in controlling telomere elongation by repressing HeT-A promoter activity. Modulation of this repression by the homolog may thus regulate telomere elongation.
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Denisenko, Oleg, and Karol Bomsztyk. "Yeast hnRNP K-Like Genes Are Involved in Regulation of the Telomeric Position Effect and Telomere Length." Molecular and Cellular Biology 22, no. 1 (January 1, 2002): 286–97. http://dx.doi.org/10.1128/mcb.22.1.286-297.2002.
Abstract:
ABSTRACT Mammalian heterogeneous nuclear ribonucleoprotein K (hnRNP K) is an RNA- and DNA-binding protein implicated in the regulation of gene expression processes. To better understand its function, we studied two Saccharomyces cerevisiae homologues of the human hnRNP K, PBP2 and HEK2 (heterogeneous nuclear RNP K-like gene). pbp2Δ and hek2Δ mutations inhibited expression of a marker gene that was inserted near telomere but not at internal chromosomal locations. The telomere proximal to the ectopic marker gene became longer, while most of the other telomeres were not altered in the double mutant cells. We provide evidence that telomere elongation might be the primary event that causes enhanced silencing of an adjacent reporter gene. The telomere lengthening could, in part, be explained by the inhibitory effect of hek2Δ mutation on the telomeric rapid deletion pathway. Hek2p was detected in a complex with chromosome regions proximal to the affected telomere, suggesting a direct involvement of this protein in telomere maintenance. These results identify a role for hnRNP K-like genes in the structural and functional organization of telomeric chromatin in yeast.
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Biessmann, Harald, Sudha Prasad, Marika F. Walter, and James M. Mason. "Euchromatic and heterochromatic domains at Drosophila telomeres." Biochemistry and Cell Biology 83, no. 4 (August 1, 2005): 477–85. http://dx.doi.org/10.1139/o05-053.
Abstract:
Noncoding repetitive sequences make up a large portion of eukaryotic genomes, but their function is not well understood. Large blocks of repetitive DNA-forming heterochromatin around the centromeres are required for this region to function properly, but are difficult to analyze. The smaller regions of heterochromatin at the telomeres provide an opportunity to study their DNA and protein composition. Drosophila telomere length is maintained through the targeted transposition of specific non-long terminal repeat retrotransposons to chromosome ends, where they form long tandem arrays. A subterminal telomere-associated sequence (TAS) lies immediately proximal to the terminal-retrotransposon array. Here, we review the experimental support for the heterochromatic features of Drosophila telomeres, and provide evidence that telomeric regions contain 2 distinct chromatin subdomains: TAS, which exhibits features that resemble beta heterochromatin; and the terminal array of retrotransposons, which appears euchromatic. This organization is significantly different from the telomeric organization of other eukaryotes, where the terminal telomerase-generated repeats are often folded in a t-loop structure and become part of the heterochromatin protein complex.Key words: Drosophila, telomere, gene silencing, position effect, heterochromatin.
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Suzuki, Y., and M. Nishizawa. "The yeast GAL11 protein is involved in regulation of the structure and the position effect of telomeres." Molecular and Cellular Biology 14, no. 6 (June 1994): 3791–99. http://dx.doi.org/10.1128/mcb.14.6.3791-3799.1994.
Abstract:
GAL11 is an auxiliary transcription factor that functions either positively or negatively, depending on the structure of the target promoters and the combination of DNA-bound activators. In this report, we demonstrate that a gal11 delta mutation caused a decrease in the length of the telomere C1-3A tract, a derepression of URA3 when it is placed next to telomere, and an increase in accessibility of the telomeric region to dam methylase, indicating that GAL11 is involved in the regulation of the structure and the position effect of telomeres. The defective position effect in a gal11 delta strain was suppressed by overproduction of SIR3, whereas overexpression of GAL11 failed to restore the telomere position effect in a sir3 delta strain. Hyperproduced GAL11 could partially suppress the defect in silencing at HMR in a sir1 delta mutant but not that in a sir3 delta mutant, suggesting that GAL11 can replace SIR1 function partly in the silencing of HMR. Overproduced SIR3 also could restore silencing at HMR in sir1 delta cells. In contrast, SIR1 in a multicopy plasmid relieved the telomere position effect, especially in a gal11 delta mutant. Since chromatin structure is thought to play a major role in the silencing at both the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by modulating the chromatin structure.
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Suzuki, Y., and M. Nishizawa. "The yeast GAL11 protein is involved in regulation of the structure and the position effect of telomeres." Molecular and Cellular Biology 14, no. 6 (June 1994): 3791–99. http://dx.doi.org/10.1128/mcb.14.6.3791.
Abstract:
GAL11 is an auxiliary transcription factor that functions either positively or negatively, depending on the structure of the target promoters and the combination of DNA-bound activators. In this report, we demonstrate that a gal11 delta mutation caused a decrease in the length of the telomere C1-3A tract, a derepression of URA3 when it is placed next to telomere, and an increase in accessibility of the telomeric region to dam methylase, indicating that GAL11 is involved in the regulation of the structure and the position effect of telomeres. The defective position effect in a gal11 delta strain was suppressed by overproduction of SIR3, whereas overexpression of GAL11 failed to restore the telomere position effect in a sir3 delta strain. Hyperproduced GAL11 could partially suppress the defect in silencing at HMR in a sir1 delta mutant but not that in a sir3 delta mutant, suggesting that GAL11 can replace SIR1 function partly in the silencing of HMR. Overproduced SIR3 also could restore silencing at HMR in sir1 delta cells. In contrast, SIR1 in a multicopy plasmid relieved the telomere position effect, especially in a gal11 delta mutant. Since chromatin structure is thought to play a major role in the silencing at both the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by modulating the chromatin structure.
Dissertations / Theses on the topic "Telomere Position Effect":
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Rey-Millet, Martin. "Les télomères, des éléments de régulation de la transcription dans les cellules sénescentes." Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ6022.
Abstract:
Les télomères sont des structures nucléoprotéiques, localisés à l’extrémité de l’ADN des cellules eucaryotes, qui préservent l’intégrité des chromosomes. Ces structures subissent des changements au cours du développement et du vieillissement, comme un raccourcissement de leurs tailles ou une altération dans leur composition en protéines (notamment le complexe shelterin). Cependant, les télomères n’ont pas qu’une fonction protectrice et peuvent aussi réguler l’expression des gènes présent dans les régions adjacentes, i.e. subtélomères, voir plus distantes. Ce processus est connu comme l’Effet de Position Télomérique (TPE), découvert initialement chez la levure Saccaromyces cerevisiae, puis chez la drosophile et Schizosaccharomyces pombe et plus récemment chez l’humain. Dans ces organismes, les gènes situés en position subtélomérique sont réprimés par un mécanisme épigénétique qui est dépendant de la taille des télomères et des protéines les composant ainsi que des structures tridimensionnelles adoptées par la chromatine télomérique et subtélomérique. Le TPE peut être décrit comme un mécanisme de propagation de l’hétérochromatine, du télomère vers le centromère, accompagné de boucle de chromatine permettant d’étendre la répression de la transcription dans des régions plus interne.Dans ce contexte, le but de ma thèse est de déterminer l’impact des télomères sur les changements transcriptionnels observés lors de la sénescence cellulaire. A cette fin, nous avons séquencé les ARNm de fibroblastes de poumon (MRC-5) jeunes et sénescents (RNAseq). Nous avons observé un enrichissement subtelomérique des gènes dont l’expression est augmentée en sénescence. Ce résultat suggère une levée de la répression induite par le TPE à la sénescence. Cette dérépression ne concerne que certains gènes et certains subtélomères.Nous avons aussi testé l’hypothèse que les protéines shelterin puissent prendre part au TPE, notamment TRF2 (Telomeric Repeat Binding Factor 2) dont l’expression est diminuée à la senescence. Nous avons donc augmenté le niveau d’expression de TRF2 dans les cellules sénescentes. Ainsi, nous avons pu observer que TRF2 modulait l’expression de certains gènes subtélomériques dans les cellules sénescentes. Par 3D-FISH, nous avons montré que cet effet de TRF2 s’accompagnait d’un remodelage spatial des subtélomères.Dans son ensemble, ce travail révèle la contribution des télomères au programme transcriptionnel des cellules sénescentes et jette ainsi les bases de l’importance du TPE dans le processus de la senescenceTelomeres, the nucleoprotein structures located at the end of eukaryotic DNA, protect chromosomal integrity. These structures undergo changes during development and aging, including length shortening and alterations in the levels of the proteins associated to them called sheltering, all this affecting genome stability as the cells age. However, telomeres also behave as transcriptional regulators acting not only on genes present at subtelomeres but also on more distantly located genes presented throughout the genome. This process is referred as Telomere Position Effect (TPE) and was initially discovered in budding yeast, but also seen in drosophila, fission yeast, plasmodium and more recently in humans. In all these organisms, genes located in the subtelomeres are repressed by an epigenetic mechanism that is dependent on telomere DNA length, telomere nucleoprotein composition and higher order chromatin organization adopted by telomeres and subtelomeres. The TPE mechanism can be described as the spreading of a heterochromatin-like structure toward the centromere most likely accompanied by the formation of large chromatin loops to further extend the transcriptional regulation emanating from a telomere to genes internally located.In this context, the goal of my thesis is to decipher whether telomeres are involved in the transcriptional remodelling occurring in human cellular senescence. For that, we performed RNA-sequencing in young versus replicative senescent lung fibroblast MRC-5 cells. Interestingly, we found an enrichment of upregulated genes in the subtelomeric regions of senescent cells suggesting a TPE alleviation. This alleviation is not homogeneous in the genome, as only some subtelomeres were enriched in upregulated genes at senescence.Finally, we tested the hypothesis that shelterin proteins may also be part of the TPE regulation. For that, we re-stored the levels of the shelterin protein TRF2 (Telomeric Repeat Binding Factor 2) whose expression is decreased as the cells approach senescence. We found that TRF2 is indeed modulating the expression of subtelomeric genes in senescent cells, and this is in part mediated by a long-range chromatin reorganization of subtelomeres as observed by conformation changes in 3D chromatin conformation by FISH.Overall, this work reveals the contribution of telomeres in the transcriptional program of senescent cells and set the basis for the relevance of TPE in the senescence/aging process
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Schulz, Vera [Verfasser]. "Identifizierung von Kandidatengenen für einen "Telomer-Positions-Effekt" beim Hutchinson-Gilford-Progerie Syndrom / Vera Schulz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1043196927/34.
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Jedrusik-Bode, Monika. "Molekulare Analyse der differentiellen Funktionen von Linkerhiston-Isoformen bei Caenorhabditis elegans." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=964334933.
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Baur, Joseph Anthony. "Telomere position effect in human cells." 2003. http://edissertations.library.swmed.edu/pdf/baurJ032003/BaurJoseph.pdf.
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"Functional studies of the C-terminal domain of Sir3 (CTD) and histone H2A in telomeric position effect (TPE)." Tulane University, 2006.
Abstract:
Heterochromatin is nucleated at a specific site and spreads into adjacent sequences through interaction between modified histories and non-histone proteins. In the yeast Saccharomyces cerevisiae, these non-histone proteins are Sir2, Sir3, and Sir4. We have previously used a tethered silencing assay to isolate the C-terminal domain 144 amino acids of Sir3 (CTD) that, when tethered adjacent to telomere, is able to restore the silencing defect conferred by the rap1-17 allele that encodes a C-terminal truncation of Rap1. Here, we explore the function and structure of CTD involving in the nucleation of silent chromatin. We demonstrate that CTD is the minimum Sir3 dimerization domain that is conserved in divergent yeasts. The CTD is able to recruit Sir2, Sir3, and Sir4 at tethering sites and to spread Sir proteins into adjacent sequences. However, the CTD-Sir3 interaction is not sufficient to restore tethered silencing because a specific CTD mutation is severely defective in tethered silencing despite its ability to recruit Sir3. In addition, CTD is able to facilitate deacetylated H4-K16. Our data suggest that cooperative interactions between CTD, Sir3p, and deacetylated H4-K16 are essential to nucleate silent chromatin. Furthermore, the sequence alignment predicts that the CTD has a Cdc6 domain III winged-helix structure found in many transcription and replication, proteins, including Orc1. Consistent with the prediction, insertion mutations in the junction of CTD abrogate silencing, suggesting that the projection of CTD toward its interaction partners is critical for Sir3 function. Interestingly, tethering of the corresponding C-terminus of Orc1 confers significant, albeit low levels, of silencing. Our results suggest that Sir3 and Orc1p may derive from the same ancestral gene Additionally, we have isolated histone H2A alleles, hta1tpe, which are defective in telomeric position effect (TPE) and the nonhomologous end joing (NHEJ) repair pathway, and confer Spt- phenotype, suggesting that hta1tpe alleles may change subtelomeric chromatin structure, resulting in impairment to recruit silencing or repair factorsacase@tulane.edu
Books on the topic "Telomere Position Effect":
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Aparicio, Oscar Martin. Telomeric position effect in S. cerevisiae: A model for the establishment of alternative transcriptional states under epigenetic control. 1993.
Book chapters on the topic "Telomere Position Effect":
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"Telomere Position Effect." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1944. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_16774.
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"Telomere Position Effect." In Encyclopedia of Gerontology and Population Aging, 4974. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_302380.
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Kipling, David. "Chromatin structure and position effects." In The Telomere, 146–67. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780199634675.003.0008.
Abstract:
Abstract In Saccharomyces cerevisiae telomeric DNA sequences can influence the expression of genes located close to them, and may also influence the timing of replication of adjacent genomic regions. Genetic analysis has revealed that this position effect on gene expression is closely related to the transcriptional repression that occurs at the silent mating-type loci. Because the latter has been characterized in great detail it will be described first, thus enabling telomere position effects to be reviewed in context.
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"Telomere Position Effect and the Evolution of the Genome." In Origin and Evolution of Telomeres, 146–60. CRC Press, 2008. http://dx.doi.org/10.1201/9781498713498-14.
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Pecorino, Lauren. "Regulation of gene expression." In Molecular Biology of Cancer. Oxford University Press, 2021. http://dx.doi.org/10.1093/hesc/9780198833024.003.0003.
Abstract:
This chapter analyzes the molecular components involved in gene expression, including transcription factors, chromatin modifications and chromatin-binding proteins, non-coding RNAs (ncRNAs), and telomeres, and how they can contribute to the processes underpinning cancer. It emphasizes that gene expression may be modulated in various ways: through the regulation of transcription, chromatin structure, and post-transcriptional mechanisms. The chapter also describes the structure of a gene within the context of chromatin in order to elucidate how gene and chromatin structure affects gene expression. Next, the chapter displays the roles of ncRNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) that play a role in gene regulation, including post-transcriptional gene expression. It also assesses the effect of telomere position and length on gene expression.
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"Telomeric Silencing (telomeric position effect)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1946. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_16780.
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Beaumont, David. "Physical Health—Te Taha Tinana." In Positive Medicine, 111–20. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780192845184.003.0009.
Abstract:
The Māori model of health considers physical health as the cornerstone of Western medicine. Maslow’s understanding of homeostasis. Seligman’s PERMA model and vitality. The relationship between vitality and ageing, and the author’s experience after a heart attack: ‘You look like an old man.’ Telomeres, stress, and ageing—‘you are only as old as you feel’. Professor Elizabeth Blackburn (and her PhD student Carol Greider)’s Nobel Prize-winning research on telomerase. The concept of healthspan. Lifestyle choices and optimum health and wellbeing. Epigenetics and Dr David Sinclair’s book, Lifespan: Why We Age – and Why We Don’t Have To. Sir Harry Burns on the role of the environment and Glasgow effect. Tertiary prevention and the author’s experience. The science of nutrition and diet. The work of Professor Grant Schofield, author of What the Fat? and What the Fast?, who promotes a healthy fat, Mediterranean diet, with low carbohydrates and intermittent fasting. The science of sleep and its role in obesity.
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Braunstein, Miriam, Scott G. Holmes,, and James R. Broach. "Heterochromatin and regulation of gene expression in. Saccharomyces cerevisiae." In Nuclear Organization, Chromatin Structure, and Gene Expression, 250–75. Oxford University PressOxford, 1997. http://dx.doi.org/10.1093/oso/9780198549239.003.0015.
Abstract:
Abstract Heterochromatin was defined by Heitz in 1928 as those chromosomal regions or entire chromosomes that remain in a condensed state throughout the cell cycle (Heitz 1928; John 1988). This definition is cytological and therefore only applicable to organisms in which individual chromosomes can be visualized. However, heterochromatin also exerts a characteristic transcriptional effect, which permits its detection and analysis even in the absence of cytological cues. Specifically, heterochromatin can exert transcriptional repression in a position-specific but gene-nonspecific manner, a process that contrasts with examples of transcriptional repression involving sequence-specific DNA binding repressor proteins and gene-specific promoter elements. The molecular basis of this heterochromatin-promoted repression remains to be determined, but likely results from exclusion of the transcriptional apparatus from the compacted chromatin structure of heterochromatin. Two examples of position effects on transcription exist in the yeast Saccharomyces cerevisiae: the silent mating-type cassettes and telomeres. Substantial evidence exists indicating that these position effect loci are enshrouded in the yeast equivalent of metazoan heterochromatin. In this chapter we will examine how studies of these position effect loci in yeast have enhanced our knowledge of what produces and comprises heterochromatin and how heterochromatin elicits transcriptional repression.
Conference papers on the topic "Telomere Position Effect":
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Tempaku, P. F., V. D'Almeida, S. M. A. Silva, L. Bittencourt, S. I. Belangero, and S. Tufik. "Effect of Continuous Positive Airway Pressure on Telomere Length and Its Associated Mechanisms." In XIX Congresso Brasileiro do Sono. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1770238.