| Range |
50-200 base pairs
|
| Organism |
Human Homo sapiens |
| Reference |
Jegou T, Chung I, Heuvelman G, Wachsmuth M, Görisch SM, Greulich-Bode KM, Boukamp P, Lichter P, Rippe K. Dynamics of telomeres and promyelocytic leukemia nuclear bodies in a telomerase-negative human cell line. Mol Biol Cell. 2009 Apr20(7):2070-82 p.2070 left columnPubMed ID19211845
|
| Primary Source |
Harley CB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature. 1990 May 31 345(6274):458-60. AND Martens UM, Chavez EA, Poon SS, Schmoor C, Lansdorp PM. Accumulation of short telomeres in human fibroblasts prior to replicative senescence. Exp Cell Res. 2000 Apr 10 256(1):291-9.PubMed ID10739676, 2342578
|
| Method |
(Primary source, Martens et al.) In order to study the mechanism(s) by which telomere shortening signals cell senescence, researchers analyzed the telomere length at specific chromosome ends at cumulative population doublings in polyclonal and clonal human diploid fibroblasts (HDFs) by quantitative fluorescence in situ hybridization. |
| Comments |
P.2070 left column: "Because of incomplete DNA synthesis at the chromosome ends, 50 –200 base pairs of telomeric DNA are lost during each replication cycle (Harley et al., 1990 Martens et al., 2000)." The loss of telomere repeats has been causally linked to in vitro replicative senescence of human diploid fibroblasts (HDFs). See Aravinthan 2015 PMID 25690721 p.52 right column 3rd paragraph: "Each cell division leads to gradual shortening of telomeres in somatic cells [ref 26], partly due to a lack of telomerase, at a rate of 30–200 bp per cell division [refs 21, 26, 27]." |
| Entered by |
Uri M |
| ID |
104276 |