Article

Protection and replication of telomeres in fission yeast

Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, 900 S. Ashland Ave. MC669, Chicago, IL 60607, USA.
Biochemistry and Cell Biology (Impact Factor: 2.15). 10/2009; 87(5):747-58. DOI: 10.1139/O09-037
Source: PubMed

ABSTRACT

Telomeres, the natural ends of linear chromosomes, must be protected and completely replicated to guarantee genomic stability in eukaryotic cells. However, the protected state of telomeres is not compatible with recruitment of telomerase, an enzyme responsible for extending telomeric G-rich repeats during S-phase; thus, telomeres must undergo switches from a protected state to an accessible state during the cell cycle. In this minireview, we will summarize recent advances in our understanding of proteins involved in the protection and replication of telomeres, and the way these factors are dynamically recruited to telomeres during the cell cycle. We will focus mainly on recent results from fission yeast Schizosaccharomyces pombe, and compare them with results from budding yeast Saccharomyces cerevisiae and mammalian cell studies. In addition, a model for the way in which fission yeast cells replicate telomeres will be presented.

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Available from: Toru M Nakamura
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    • "Therefore, the interaction between the proteins TPP1 and TIN2 forms the keystone of the bridge between ss-DNA and ds-DNA. A similar organization is found in the terminal Schizosaccharomyces pombe complex that also contains six proteins (reviewed in Moser and Nakamura, 2009). "
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    ABSTRACT: A major issue in telomere research is to understand how the integrity of chromosome ends is controlled. The fact that different types of nucleoprotein complexes have been described at the telomeres of different organisms raises the question of whether they have in common a structural identity that explains their role in chromosome protection. We will review here how telomeric nucleoprotein complexes are structured, comparing different organisms and trying to link these structures to telomere biology. It emerges that telomeres are formed by a complex and specific network of interactions between DNA, RNA, and proteins. The fact that these interactions and associated activities are reinforcing each other might help to guarantee the robustness of telomeric functions across the cell cycle and in the event of cellular perturbations. We will also discuss the recent notion that telomeres have evolved specific systems to overcome the DNA topological stress generated during their replication and transcription. This will lead to revisit the way we envisage the functioning of telomeric complexes since the regulation of topology is central to DNA stability, replication, recombination, and transcription as well as to chromosome higher-order organization.
    Full-text · Article · Mar 2013 · Frontiers in Oncology
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    • "Heterochromatin formation has an important function also for telomere capping in Schizosaccharomyces pombe. In this organism , telomere protection is assured by a complex of shelterinlike proteins (Moser and Nakamura, 2009). In the absence of telomerase, S. pombe cells can survive telomere loss by adopting an alternative mode to protect chromosome ends based on amplification and rearrangement of heterochromatic regions (Jain et al., 2010). "
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    ABSTRACT: The establishment of a specific nucleoprotein structure, the telomere, is required to ensure the protection of chromosome ends from being recognized as DNA damage sites. Telomere shortening below a critical length triggers a DNA damage response that leads to replicative senescence. In normal human somatic cells, characterized by telomere shortening with each cell division, telomere uncapping is a regulated process associated with cell turnover. Nevertheless, telomere dysfunction has also been associated with genomic instability, cell transformation, and cancer. Despite the essential role telomeres play in chromosome protection and in tumorigenesis, our knowledge of the chromatin structure involved in telomere maintenance is still limited. Here we review the recent findings on chromatin modifications associated with the dynamic changes of telomeres from protected to deprotected state and their role in telomere functions.
    Full-text · Article · Mar 2013 · Frontiers in Oncology
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    • "In model organisms, telomeres have been shown to impede chromosomal fusion (end-to-end joining ) and degradation. Therefore, the absence of telomeres in these organisms results in genetic instability and loss of cellular viability [14,15]. Telomeric DNA is arranged in short tandem sequence repeats containing groups of three or four guanines (e.g., TTGGGG in Tetrahymena [16] and TTAGGG in humans [17] ). "
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    ABSTRACT: In recent years, many studies have focused on heterochromatin located at chromosome ends, which plays an important role in regulating gene expression in many organisms ranging from yeast to humans. Similarly, in the protozoan Plasmodium falciparum, which is the most virulent human malaria parasite, the heterochromatin present in telomeres and subtelomeric regions exerts a silencing effect on the virulence gene families located therein. Studies addressing P. falciparum chromosome ends have demonstrated that these regions participate in other functions, such as the formation of the T-loop structure, the replication of telomeric regions, the regulation of telomere length and the formation of telomeric heterochromatin. In addition, telomeres are involved in anchoring chromosome ends to the nuclear periphery, thereby playing an important role in nuclear architecture and gene expression regulation. Here, we review the current understanding of chromosome ends, the proteins that bind to these regions and their impact on the biology and virulence of P. falciparum.
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