DNA excision repair at telomeres

Jia, Pingping; Her, Chengtao; Chai, Weihang

doi:10.1016/j.dnarep.2015.09.017

Cited by 40 publications

(38 citation statements)

References 120 publications

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“…Second, processes that accelerate telomere shortening may also hasten the accumulation of damage to other biomolecules in somatic tissues. For example, oxidative damage can accelerate telomere shortening directly by causing breaks in telomeric DNA, the repair of which may be suppressed to some extent (Jia, Her, & Chai, ; Kawanishi & Oikawa, ; Petersen, Saretzki, & Zglinicki, ; Von Zglinicki, ). Telomere shortening could thereby reflect the correlated accumulation of oxidative damage to other biomolecules in somatic tissues.…”

Section: Introductionmentioning

confidence: 99%

Telomere attrition predicts reduced survival in a wild social bird, but short telomeres do not

Wood

Young

2019

Molecular Ecology

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Attempts to understand the causes of variation in senescence trajectories would benefit greatly from biomarkers that reflect the progressive declines in somatic integrity (SI) that lead to senescence. While telomere length has attracted considerable interest in this regard, sources of variation in telomere length potentially unrelated to declines in SI could, in some contexts, leave telomere attrition rates a more effective biomarker than telomere length alone. Here, we investigate whether telomere length and telomere attrition rates predict the survival of wild white‐browed sparrow‐weaver nestlings (Plocepasser mahali). Our analyses of telomere length reveal counterintuitive patterns: telomere length soon after hatching negatively predicted nestling survival to fledging, a pattern that appears to be driven by differentially high in‐nest predation of broods with longer telomeres. Telomere length did not predict survival outside this period: neither hatchling telomere length nor telomere length in the mid‐nestling period predicted survival from fledging to adulthood. Our analyses using within‐individual telomere attrition rates, by contrast, revealed the expected relationships: nestlings that experienced a higher rate of telomere attrition were less likely to survive to adulthood, regardless of their initial telomere length and independent of effects of body mass. Our findings support the growing use of telomeric traits as biomarkers of SI, but lend strength to the view that longitudinal assessments of within‐individual telomere attrition since early life may be a more effective biomarker in some contexts than telomere length alone.

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Section: Introductionmentioning

confidence: 99%

Telomere attrition predicts reduced survival in a wild social bird, but short telomeres do not

Wood

Young

2019

Molecular Ecology

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“…The telomeric sequence possesses unique features (e.g., long, tandem G‐rich repeats) that predispose telomeres to a variety of DNA damage from intracellular metabolic processes such as hydrolysis, oxidative alkylation and DNA base mismatches, as well as by insult from exogenous sources, which will not be included in this study (e.g., UV light; Jia, Her, & Chai, ). To protect genomic stability, Metazoan cells have evolved highly conserved DNA repair mechanisms to remove and repair such DNA lesions (Ahmed & Lingner, ; Jia et al., ; Kansara & Gupta, ; Tan et al., ). One group of repair pathways for telomeric maintenance is excision and repair of bases (BER), nucleotides (NER) and DNA mismatches (MMR).…”

Section: Introductionmentioning

confidence: 99%

“…One group of repair pathways for telomeric maintenance is excision and repair of bases (BER), nucleotides (NER) and DNA mismatches (MMR). BER is a cellular mechanism that corrects discrete, small DNA base lesions caused by oxidative deamination and, when defective, can elevate mutation rate and cancer risk (Jia et al., ).…”

Section: Introductionmentioning

confidence: 99%

Long‐term effects of superoxide and DNA repair on lizard telomeres

et al. 2018

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Telomeres are the non-coding protein-nucleotide "caps" at chromosome ends that contribute to chromosomal stability by protecting the coding parts of the linear DNA from shortening at cell division, and from erosion by reactive molecules. Recently, there has been some controversy between molecular and cell biologists, on the one hand, and evolutionary ecologists on the other, regarding whether reactive molecules erode telomeres during oxidative stress. Many studies of biochemistry and medicine have verified these relationships in cell culture, but other researchers have failed to find such effects in free-living vertebrates. Here, we use a novel approach to measure free radicals (superoxide), mitochondrial "content" (a combined measure of mitochondrial number and size in cells), telomere length and DNA damage at two primary time points during the mating season of an annual lizard species (Ctenophorus pictus). Superoxide levels early in the mating season vary widely and elevated levels predictshorter telomeres both at that time as well as several months later. These effects are likely driven by mitochondrial content, which significantly impacts late season superoxide (cells with more mitochondria have more superoxide), but superoxide effects on telomeres are counteracted by DNA repair as revealed by 8-hydroxy-2′-deoxyguanosine assays. We conclude that reactive oxygen species and DNA repair are fundamental for both short-and long-term regulation of lizard telomere length with pronounced effects of early season cellular stress detectable on telomere length near lizard death. K E Y W O R D S Ctenophorus pictus, flow FISH, mitochondrial mass, qPCR, superoxide, telomeresThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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“…This kind of senescence is intuitively linked with changes in telomere length and structure (uncapping), and therefore, is also recognized as telomere-dependent senescence. Telomeric ends are particularly prone to DNA damage, mostly single-strand breaks (SSB) and double-strand breaks (DBS), due to defective DNA repair mechanisms [33]. Gradual decomposition of telomeres through shortening and/or uncapping induces the DNA damage response (DDR) pathway [34], which is responsible for a cell evacuating from the cell cycle.…”

Section: Mechanismsmentioning

confidence: 99%

Mechanisms and significance of therapy-induced and spontaneous senescence of cancer cells

Mikuła-Pietrasik

Niklas

Uruski

et al. 2019

Cell. Mol. Life Sci.

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In contrast to the well-recognized replicative and stress-induced premature senescence of normal somatic cells, mechanisms and clinical implications of senescence of cancer cells are still elusive and uncertain from patient-oriented perspective. Moreover, recent years provided multiple pieces of evidence that cancer cells may undergo senescence not only in response to chemotherapy or ionizing radiation (the so-called therapy-induced senescence) but also spontaneously, without any external insults. Since the molecular nature of the latter process is poorly recognized, the significance of spontaneously senescent cancer cells for tumor progression, therapy effectiveness, and patient survival is purely speculative. In this review, we summarize the most up-to-date research regarding therapy-induced and spontaneous senescence of cancer cells, by delineating the most important discoveries regarding the occurrence of these phenomena in vivo and in vitro. This review provides data collected from studies on various cancer cell models, and the narration is presented from the broader perspective of the most critical findings regarding the senescence of normal somatic cells.

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DNA excision repair at telomeres

Cited by 40 publications

References 120 publications

Telomere attrition predicts reduced survival in a wild social bird, but short telomeres do not

Telomere attrition predicts reduced survival in a wild social bird, but short telomeres do not

Long‐term effects of superoxide and DNA repair on lizard telomeres

Mechanisms and significance of therapy-induced and spontaneous senescence of cancer cells

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