scholarly journals Reply to Udroiu: Interesting mathematical analysis of telomere shortening rate and life span

2020 ◽  
Vol 117 (5) ◽  
pp. 2250-2250
Author(s):  
Kurt Whittemore ◽  
Maria A. Blasco
2004 ◽  
Vol 279 (17) ◽  
pp. 17826-17833 ◽  
Author(s):  
Carmen Martin-Ruiz ◽  
Gabriele Saretzki ◽  
Joanne Petrie ◽  
Juliane Ladhoff ◽  
Jessie Jeyapalan ◽  
...  

2019 ◽  
Vol 116 (30) ◽  
pp. 15122-15127 ◽  
Author(s):  
Kurt Whittemore ◽  
Elsa Vera ◽  
Eva Martínez-Nevado ◽  
Carola Sanpera ◽  
Maria A. Blasco

Telomere shortening to a critical length can trigger aging and shorter life spans in mice and humans by a mechanism that involves induction of a persistent DNA damage response at chromosome ends and loss of cellular viability. However, whether telomere length is a universal determinant of species longevity is not known. To determine whether telomere shortening can be a single parameter to predict species longevities, here we measured in parallel the telomere length of a wide variety of species (birds and mammals) with very different life spans and body sizes, including mouse (Mus musculus), goat (Capra hircus), Audouin’s gull (Larus audouinii), reindeer (Rangifer tarandus), griffon vulture (Gyps fulvus), bottlenose dolphin (Tursiops truncatus), American flamingo (Phoenicopterus ruber), and Sumatran elephant (Elephas maximus sumatranus). We found that the telomere shortening rate, but not the initial telomere length alone, is a powerful predictor of species life span. These results support the notion that critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.


2021 ◽  
Author(s):  
Tiia Karkkainen ◽  
Toni Laaksonen ◽  
Malcolm Burgess ◽  
Alejandro Cantarero ◽  
Jesus Martinez-Padilla ◽  
...  

Telomere length and shortening rate are increasingly used as biomarkers for long-term costs in ecological and evolutionary studies because of their relationships with survival and fitness. Telomere length can be heritable, but both early-life conditions and later-life stressors can create variation in telomere shortening rate. Studies on between-population telomere length and dynamics are mostly lacking, despite the expectation that populations exposed to varying environmental constraints would present divergent telomere length patterns. Pied flycatcher (Ficedula hypoleuca) is a passerine bird spending the non-breeding period in sub-Saharan Africa but breeding across Eurasia (from Spain to western Siberia). Populations show marked differences in migration distance, genetics, breeding parameters, and egg components. We studied the large-scale variation of telomere length, early-life dynamics and heritability in the pied flycatcher by comparing six European populations across a north-south gradient (Finland, Estonia, England and Spain). There were clear population differences in telomere length, with English birds having the longest telomeres, followed by Spanish and lastly by Estonian and Finnish birds. Early-life telomere shortening rate tended to vary between populations, and faster nestling growth affected telomeres more negatively in northern than southern populations. The heritability of telomere length was moderate (h2 = 0.34 - 0.40), with stronger heritability to paternal than maternal telomere length. There was also evidence indicating that the level of paternal heritability could differ between populations. While the sources of between-population differences in telomere-related biology remain to be identified (i.e. genetics, environmental factors), our study illustrates the need to expand telomere studies at the between-population level.


1978 ◽  
Vol 40 (01) ◽  
pp. 083-088 ◽  
Author(s):  
E Dassin ◽  
Y Najean ◽  
O Poirier ◽  
Ph Passa ◽  
D Bensoussan

SummaryIn vivo platelet survival was estimated, in 31 diabetic patients, using 51Cr-labelled autologous platelets. A mathematical analysis attempted to measure the “potential” life span (senescence process) and the degree of a superimposed aleatory destruction (consumption process).The potential platelet life span in diabetics did not differ from normal values. However, excessive consumption was observed in one third of the studied cases, without correlation with the age of the patients, the clinical duration of diabetes, and the degree of vascular impairment. Thus, platelet kinetic studies did not provide presently useful indications, in a particular patient, regarding the prognosis of the vascular disease, and the justification of anti-aggregant therapy.


2020 ◽  
Vol 21 (7) ◽  
pp. 2520 ◽  
Author(s):  
Olga Utyro ◽  
Joanna Perła-Kaján ◽  
Hieronim Jakubowski

Cystathionine β-synthase (CBS) is a housekeeping enzyme that catalyzes the first step of the homocysteine to cysteine transsulfuration pathway. Homozygous deletion of the Cbs gene in mice causes severe hyperhomocysteinemia and reduces life span. Here, we examined a possible involvement of senescence, mitochondrial DNA, and telomeres in the reduced life span of Cbs−/− mice. We found that senescence-related p21, Pai-1, Mcp1, and Il-6 mRNAs were significantly upregulated (2–10-fold) in liver, while p21 was upregulated in the brain of Cbs−/− mice (n = 20) compared with control Cbs+/− siblings (n = 20) in a sex- and age-dependent manner. Telomere length in blood (n = 80), liver (n = 40), and brain (n = 40) was not affected by the Cbs−/− genotype, but varied with sex and/or age. Levels of mitochondrial DNA tended to be reduced in livers, but not brains and blood, of Cbs−/− females (n = 20–40). The Cbs−/− genotype significantly reduced Tert mRNA expression in brain, but not liver, in a sex- and age-dependent manner. Multiple regression analysis showed that the senescence-related liver (but not brain) mRNAs and liver (but not brain or blood) mitochondrial DNA were associated with the Cbs genotype. In contrast, telomere length in blood, brain, and liver was not associated with the Cbs genotype or hyperhomocysteinemia, but was associated with sex (in brain and liver) and age (in brain and blood). Taken together, these findings suggest that the changes in senescence marker expression and mtDNA levels, but not telomere shortening, could account for the reduced life span of Cbs−/− mice.


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