Quiz
Tap a question to see the answer
1. What did Hayflick and Moorhead show in 1961?
That normal human diploid cell strains stop dividing in culture, unlike immortal cell lines. The approximate 50 subcultivations is Serrano's 2024 summary of that paper, not a table reprinted in this lesson (Figure 1).
2. How is Olovnikov's marginotomy different from telomerase?
Marginotomy is the incomplete copying of a chromosome end. Telomerase is the enzyme that adds repeats back. Greider and Blackburn, 1985, found that activity in Tetrahymena, adding TTGGGG, not human TTAGGG (Figure 1).
3. What did Harley, Futcher, and Greider show, and what did they leave open?
Telomeres shorten as human fibroblasts are passaged. They said it was not known whether that loss causes senescence (Figure 1).
4. What did Bodnar and colleagues test?
Putting the human telomerase catalytic subunit into normal human cells lengthened telomeres and let the cultures pass their usual limit by at least 20 doublings, with a normal karyotype in that paper. It was cells in a dish (Figures 1 and 2).
5. Why are 40 to 200 base pairs and 10 doublings per kilobase not the same number?
40 to 200 is a range of loss per division in cultured human cells, from Wright and colleagues, 1997. Ten doublings per kilobase is Allsopp's regression of remaining divisions on starting length, r = 0.76 (Figure 2).
6. What does the species chart show about mice?
Laboratory mice can have very long telomeres. CAST/Ei, about 18 to 20 kb, and C57BL/6J, with long telomeres, did not differ significantly in the maximal lifespans Hemann and Greider report. Gomes and colleagues found shorter telomeres with longer mammal lifespans (Figure 3).
7. What is the cancer side of a long telomere?
Kim and colleagues found telomerase in 90 of 101 tumor biopsies and in none of 50 normal somatic tissues. Haycock and colleagues found that genetically longer telomeres raise the odds of several cancers, including glioma, and lower the odds of coronary heart disease (Figure 4).
8. What is dyskeratosis congenita doing on this figure?
It is an inherited short-telomere disease. DKC1, telomerase RNA, and short telomeres in patients' cells show that telomere failure can cause proliferative disease. It is not a measurement of ordinary aging (Figure 4).
9. What did Jaskelioff and colleagues reverse, and in which mice?
Tissue degeneration, including in the brain, after telomerase was switched back on. The mice were late-generation telomerase-deficient mice, not ordinary old wild-type mice (Figure 4).
10. Why is telomere length still contested as a clock of human aging?
The correlation with age is weak, laboratories do not agree on absolute length, mice with long telomeres are not long-lived for that reason, and senescence is also triggered by oncogenic ras. Mortality findings such as Cawthon's are associations (Figure 4).
11. What do the reading-room pages not show?
They do not show that a telomere assay, a nuclear fluctuation, or an NAD precursor produced the historical rise in population life expectancy. The measurement paper is a preprint about a method. The heart result is old male mice (Figure 5).